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| 1 | Oral berberine improves brain dopa/dopamine levels to ameliorate Parkinson’s disease by regulating gut microbiota显示文摘The phenylalanine-tyrosine-dopa-dopamine pathway provides dopamine to the brain.Iin this process,tyrosine hydroxylase(TH)isthe rate-limiting enzyme that hydroxylates tyrosine and generates levodopa(L-dopa)with tetranydrobiopterin(BH_(4))as a coenzyme.Here,we show that oral berberine(BBR)might supply H^(·) through dihydroberberine(reduced BBR produced by bacterial nitroreductase)and promote the production of BHl from dihydrobiopterin;the increased BH,enhances TH activity,which accelerates the production of L-dopa by the gut bacteria.Oral BBR acts in a way similar to vitamins.The L-dopa produced by theintestinal bacteria enters the brain through the circulation and is transformed to dopamine.To verify the gut-brain dialog activatedby BBR's effect,Enterococcus foecalis or Enterococcus faecium was transplanted into Parkinson's disease(PD)mice.The bacteriasignificantly increased brain dopamine and ameliorated PD manifestation in mice;additionally,combination of BBR with bacteriashowed better therapeutic effect than that with bacteria alone.Moreover,2,4,6-trimethy-pyranylium tetrafluoroborate(TMP-TFB)-derivatized matrix-assisted laser desorption mass spectrometry(MALDI-MS)imaging of dopamine identihed elevated striataldopamine levels in mouse brains with oral Enterococcus,and BBR strengthened the imaging intensity of brain dopamine.Theseresults demonstrated that BBR was an agonist of TH in Enterococcus and could lead to the production of L-dopa in the gut.Furthermore,a study of 28 patients with hyperlipidemia conhrmed that oral BBR increased bloodfecal L-dopa by the intestinalbacteria.Hence,BBR might improve the brain function by upregulating the biosynthesis of-dopa in the gut microbiota through avitamin-like effect. | Yan Wang Qian Tong Shu-Rong Ma Zhen-Xiong Zhao Li-Bin Pan Lin Cong Pei Han Ran Peng Hang Yu Yuan Lin Tian-Le Gao Jia-Wen Shou Xiao-Yang Li Xian-Feng Zhang Zheng-Wei Zhang Jie Fu Bao-Ying Wen Jin-Bo Yu Xuetao Cao Jian-Dong Jiang | 2021 | Signal Transduction and Targeted Therapy2021，6，3： | 16 |
| 2 | Potassium Channels: A Potential Therapeutic Target for Parkinson's Disease显示文摘The pathogenesis of the second major neurodegenerative disorder, Parkinson's disease(PD), is closely associated with the dysfunction of potassium(K^+ ) channels. Therefore, PD is also considered to be an ion channel disease or neuronal channelopathy. Mounting evidence has shown that K^+ channels play crucial roles in the regulations of neurotransmitter release, neuronal excitability, and cell volume. Inhibition of K^+ channels enhances the spontaneous firing frequency of nigral dopamine(DA)neurons, induces a transition from tonic firing to burst discharge, and promotes the release of DA in the striatum.Recently, three K^+ channels have been identified to protect DA neurons and to improve the motor and non-motor symptoms in PD animal models: small conductance(SK)channels, A-type K^+ channels, and KV7/KCNQ channels.In this review, we summarize the physiological and pharmacological effects of the three K^+ channels. We also describe in detail the laboratory investigations regarding K^+ channels as a potential therapeutic target for PD. | Xiaoyan Chen Bao Xue Jun Wang Haixia Liu Limin Shi Junxia Xie | 2018 | Neuroscience Bulletin2018，34，2： | 13 |
| 3 | The hypothalamic-spinal dopaminergic system:a target for pain modulation显示文摘Nociceptive signals conveyed to the dorsal horn of the spinal cord by primary nociceptors are subject to extensive modulation by local neurons and by supraspinal descending pathways to the spinal cord before being relayed to higher brain centers. Descending modulatory pathways to the spinal cord comprise,among others, noradrenergic, serotonergic, γ-aminobutyric acid(GABA)ergic, and dopaminergic fibers.The contributions of noradrenaline, serotonin, and GABA to pain modulation have been extensively investigated. In contrast, the contributions of dopamine to pain modulation remain poorly understood.The focus of this review is to summarize the current knowledge of the contributions of dopamine to pain modulation. Hypothalamic A11 dopaminergic neurons project to all levels of the spinal cord and provide the main source of spinal dopamine. Dopamine receptors are expressed in primary nociceptors as well as in spinal neurons located in different laminae in the dorsal horn of the spinal cord, suggesting that dopamine can modulate pain signals by acting at both presynaptic and postsynaptic targets. Here, I will review the literature on the effects of dopamine and dopamine receptor agonists/antagonists on the excitability of primary nociceptors, the effects of dopamine on the synaptic transmission between primary nociceptors and dorsal horn neurons, and the effects of dopamine on pain in rodents. Published data support both anti-nociceptive effects of dopamine mediated by D2-like receptors and pro-nociceptive effects mediated by D1-like receptors. | Michelino Puopolo | 2019 | Neural Regeneration Research2019，14，6： | 10 |
| 4 | Modulation of TGFβ_2 and dopamine by PKC in retinal Müller cells of guinea pig myopic eye显示文摘AIM: To investigate the effect of protein kinase C (PKC) on transforming growth factor-β2 (TGFβ2) and dopamine in retinal Müller cells of guinea pig myopic eye. METHODS: Myopia was induced by translucent goggles in guinea pig, whose retinal Müller cells were cultured using the enzyme-digesting method. Retinal Müller cells were divided into 5 groups: normal control, myopia, myopia plus GF109203X, myopia plus PMA, myopia plus DMSO. PKC activities were detected by the non-radioactive methods. TGFβ2 and tyrosine hydroxylase (TH) proteins were analyzed by Western Blotting in retinal Müller cells. Dopamine was determined by the high-performance liquid chromatography- electrochemical detection in suspensions. RESULTS: After 14 days deprived, the occluded eyes became myopic with ocular axle elongating. Müller cells of guinea pigs were obtained using enzyme digestion. Compared with normal control group, the increase in PKC activity and the up-regulation in TGFβ2 expression were found in retinal Müller cells of myopic eyes, with the decrease of TH and dopamine content (P <0.05). After PKC activated by PMA, TGFβ2 and TH content were up-regulated with the increase of dopamine content (P <0.05). While the PKC activities was inhibited by GF109203X, proteins of TGFβ2 and TH were down-regulated in the myopic eyes, with the decrease of dopamine content (P <0.05). CONCLUSION: TGFβ2 and dopamine are modulated by PKC in Müller cells of the myopic eyes in guinea pig. | Jun-Feng Mao, Shuang-Zhen Liu, Wen-Juan Qin, Qian Xiang Department of Ophthalmology, Xiangya Hospital of Central South University, Changsha 410008, Hunan Province, China | 2011 | International Journal of Ophthalmology(English edition)2011，4，4： | 10 |
| 5 | Toosendanin-induced change of dopamine level detected by microdialysis in vivo at rat striatum显示文摘To investigate the effect on central nervous transmission of toosendanin (TSN), a presynaptic blocker, rat striatum was perfused in vivo with a TSN-containing artificial cere-brospinal fluid (ACSF) and the level of dopamine (DA) as well as related metabolites in the collected dialysates has been determined by a microbore HPLC with electrochemical detection (mi-crobore HPLC-ECD). The results are as follows: ( i ) TSN induced a biphasic change of DA from its basal level;( ii ) the basal contents of two metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) increased in turn and stayed at a higher level than basal control for a long period. The basal level of 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of 5-hydroxytryptamine(5-HT), had a change similar to that of HVA; (iii) after per-fusion with TSN-containing ACSF, high K+-evoked DA release was inhibited. These results show that TSN does not selectively affect acetylcholine (ACh) release, but probably acts on a common | Wenyan Chen Pingbo Yin Weiling Ye Yuliang Shi | 1999 | Chinese Science Bulletin1999，44，12： | 10 |
| 6 | 多巴胺肾保护及抗休克作用的再认识显示文摘多年来,多巴胺(dopamine,DA)因其"不同剂量作用于不同受体并发挥不同效应"的药效学特点得以在临床广泛应用。然而,随着认识的逐步深入,其肾脏保护作用及抗休克效应受到质疑,因此有必要重新审视其药理作用及临床应用。本文就DA肾脏效应及抗休克作用进行阐述,为临床医师合理使用DA提供参考。多巴胺的生理作用和临床应用现状 二十世纪50年代,DA作为儿茶酚胺家族中一种由脑内分泌合成的激素,在大脑内作为神经递质而首先被发现。 | 韩传宝 钱燕宁 | 2016 | 临床麻醉学杂志2016，32，3： | 9 |
| 7 | Ginsenoside Rb1 protects dopaminergic neurons from inflammatory injury induced by intranigral lipopolysaccharide injection显示文摘Accumulating studies suggest that neuroinflammation characterized by microglial overactivation plays a pivotal role in the pathogenesis of Parkinson’s disease.As such,inhibition of microglial overactivation might be a promising treatment strategy to delay the onset or slow the progression of Parkinson’s disease.Ginsenoside Rbl,the most active ingredient of ginseng,reportedly exerts neuroprotective effects by suppressing inflammation in vitro.The present study aimed to evaluate the neuroprotective and anti-inflammatory effects of ginsenoside Rbl in a lipopolysaccharide-induced rat Parkinson’s disease model.Rats were divided into four groups.In the control group,sham-operated rats were intraperitoneally administered normal saline for 14 consecutive days.In the ginsenoside Rbl group,ginsenoside Rb1(20 mg/kg)was intraperitoneally injected for 14 consecutive days after sham surgery.In the lipopolysaccharide group,a single dose of lipopolysaccharide was unilaterally microinjected into the rat substantial nigra to establish the Parkinson’s disease model.Lipopolysaccharide-injected rats were treated with normal saline for 14 consecutive days.In the ginsenoside Rbl +lipopolysaccharide group,lipopolysaccharide was unilaterally microinjected into the rat substantial nigra.Subsequently,ginsenoside Rbl was intraperitoneally injected for 14 consecutive days.To investigate the therapeutic effects of ginsenoside Rbl,behavioral tests were performed on day 15 after lipopolysaccharide injection.We found that ginsenoside Rbl treatment remarkably reduced apomorphine-induced rotations in lipopolysaccharide-treated rats compared with the lipopolysaccharide group.To investigate the neurotoxicity of lipopolysaccharide and potential protective effect of ginsenoside Rbl,contents of dopamine and its metabolites in the striatum were measured by high-performance liquid chromatography.Compared with the lipopolysaccharide group,ginsenoside Rbl obviously attenuated the lipopolysaccharide-induced depletion of dopamine and its metabolites in the striatum.To further explore the neuroprotective effect of ginsenoside Rbl against lipopolysaccharide-induced neurotoxicity,immunohistochemistry and western blot assay of tyrosine hydroxylase were performed to evaluate dopaminergic neuron degeneration in the substantial nigra par compacta.The results showed that lipopolysaccharide injection caused a large loss of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra and a significant decrease in overall tyrosine hydroxylase expression.However,ginsenoside Rb1 noticeably reversed these changes.To investigate whether the neuroprotective effect of ginsenoside Rbl was associated with inhibition of lipopolysaccharide-induced microglial activation,we examined expression of the microglia marker Iba-1.Our results confirmed that lipopolysaccharide injection induced a significant increase in Iba-1 expression in the substantia nigra;however,ginsenoside Rbl effectively suppressed lipopolysaccharide-induced microglial overactivation.To elucidate the inhibitory mechanism of ginsenoside Rb1,we examined expression levels of inflammatory mediators(tumor necrosis factor-a,interleukin-1β,inducible nitric oxide synthase,and cyclooxygenase 2)and phosphorylation of nuclear factor kappa B signaling-related proteins(IκB,IKK)in the substantia nigra with enzyme-linked immunosorbent and western blot assays.Our results revealed that compared with the control group,phosphorylation and expression of inflammatory mediators IκB and IKK in the substantia nigra of lipopolysaccharide group rats were significantly increased;whereas,ginsenoside Rbl obviously reduced lipopolysaccharide-induced changes on the lesioned side of the substantial nigra par compacta.These findings confirm that ginsenoside Rbl can inhibit inflammation induced by lipopolysaccharide injection into the substantia nigra and protect dopaminergic neurons,which may be related to its inhibition of the nuclear factor kappa B signaling pathway.This study was approved by the Experimental Animal Ethics Committee of Shandong University of China in April 2016(approval No.KYLL-2016-0148). | Da-Wei Li Fa-Zhan Zhou Xian-Chang Sun Shu-Chen Li Jin-Bin Yang Huan-Huan Sun Ai-Hua Wang | 2019 | Neural Regeneration Research2019，14，10： | 9 |
| 8 | Sevoflurane plays a reduced role in cognitive impairment compared with isoflurane: limited effect on fear memory retention显示文摘Isoflurane and sevoflurane are both inhalation anesthetics,but in clinical application,sevoflurane has been considered to be less suitable for long-term anesthesia because of its catabolic compounds and potential nephrotoxicity.Nevertheless,recent studies have shown that these two inhalation anesthetics are similar in hepatorenal toxicity,cost,and long-term anesthetic effect.Moreover,sevoflurane possibly has less cognitive impact on young mice.In this study,C57BL/6 mice aged 8–10 weeks were exposed to 1.2%isoflurane or 2.4%sevoflurane for 6 hours.Cognitive function and memory were examined in young mice using the novel object recognition,contextual fear conditioning,and cued-fear extinction tests.Western blot assay was performed to detect expression levels of D1 dopamine receptor,catechol-O-methyltransferase,phospho-glycogen synthase kinase-3β,and total glycogen synthase kinase-3βin the hippocampus.Our results show that impaired performance was not detected in mice exposed to sevoflurane during the novel object recognition test.Contextual memory impairment in the fear conditioning test was shorter in the sevoflurane group than the isoflurane group.Long-term sevoflurane exposure did not affect memory consolidation,while isoflurane led to memory consolidation and reduced retention.Downregulation of hippocampal D1 dopamine receptors and phosphorylated glycogen synthase kinase-3β/total glycogen synthase kinase-3βand upregulation of catechol-O-methyltransferase may be associated with differing memory performance after exposure to isoflurane or sevoflurane.These results confirm that sevoflurane has less effect on cognitive impairment than isoflurane,which may be related to expression of D1 dopamine receptors and catechol-O-methyltransferase and phosphorylation of glycogen synthase kinase-3βin the hippocampus.This study was approved by the Institutional Animal Care and Use Committee,Nanjing University,China on November 20,2017(approval No.20171102). | Ying Du Xiang-Dan Gong Xin Fang Fang Xing Tian-Jiao Xia Xiao-Ping Gu | 2020 | Neural Regeneration Research2020，15，1： | 8 |
| 9 | The cessation and detoxification effect of tea filters on cigarette smoke显示文摘To treat tobacco addiction,a tea filter was developed and studied for smoking cessation.This work reports the smoking cessation effect of tea when it was used as a component of cigarette filters.In one trial it was found that after using the tea filters for 2 months,the volunteer smokers decreased their cigarette consumption by 56.5%,and 31.7% of them stopped smoking.This work identified a new method and material,tea filter and theanine,which inhibit tobacco and nicotine addiction and provide an effective strategy for treating tobacco addiction. | YAN JingQi1,2,DI XiaoJing1,4,LIU CaiYi3,ZHANG HuiMin3,HUANG XiouQin3,ZHANG JunJing1,2,ZHAO Yan5,ZHANG LongZe1,CHANG YanZhong4,LIANG YongLin2$,TAO Ran3 & ZHAO BaoLu1,21 State Key Laboratory of Brain and Cognitive Science,Institute of Biophysics,Chinese Academy of Sciences,Beijing 100101,China 2 Key Laboratory of Mental Health,Institute of Psychology,Chinese Academy of Sciences,Beijing 100101,China 3 Addiction Branch,Beijing Military Region General Hospital,Beijing 100700,China 4 Institute of Molecular Neurobiology,Hebei Normal University,Shijiazhuang 050016,China 5 Department of Food Sciences and Technology,Harbin Institute of Technology at Weihai,Weihai 264209,China | 2010 | Science China(Life Sciences)2010，53，5： | 8 |
| 10 | Antitumor effect of axitinib combined with dopamine and PKPD modeling in the treatment of human breast cancer xenograft显示文摘Rising evidence has shown the development of resistance to vascular endothelial growth factor receptor (VEGFR) inhibitors in the practices of cancer therapy. It is reported that the efficacy of axitinib (AX), a VEGFR inhibitor, is limited in the treatment of breast cancer as a single agent or in combination with other chemotherapeutic drugs due to the probability of rising population of cancer stem-like cells (CSCs) caused by AX. The present study evaluated the effect of dopamine (DA) improving AX’s efficacy on MCF-7/ADR breast cancer in vitro and in vivo, and developed a pharmacokinetic-pharmacodynamic (PK-PD) model describing the in vivo experimental data and characterizing the interaction of effect between AX and DA. The results showed that AX up-regulated the expression of breast CSC (BCSC) markers (CD44^+/CD24^-/low) in vivo, and DA significantly synergized the inhibitory effect on tumor growth by deducting the BCSC frequency. The PK-PD model quantitatively confirmed the synergistic interaction with the parameter estimate of interaction factor ψ 2.43. The dose regimen was optimized as 60mg/kg AX i.g. b.i.d. combined with 50mg/kg DA i.p. q3d in the simulation study on the basis of the PK-PD model. The model where DA synergistically enhances the effect of AX in an all-or-none manner provides a possible solution in modeling the agents like DA. Moreover, the outcome of AX and DA combination therapy in MCF-7/ADR breast cancer provided further insight of co-administering DA in the treatment of the possible CSC-causing AX-resisting breast cancer. And this combination therapy has the prospect of clinical translation. | Yuan-heng Ma Si-yuan Wang Yu-peng Ren Jian Li Ting-jie Guo Wei Lu Tian-yan Zhou | 2019 | Acta Pharmacologica Sinica2019，40，2： | 7 |
| 11 | Corrosion protection investigations of carbon dots and polydopamine composite coating on magnesium alloy显示文摘A composite coating of nitrogen-doped carbon dots(N–CDs)and polydopamine(PDA)was prepared on magnesium alloy by combining electrodeposition with dip coating methods.The microstructure of the N–CDs/PDA composite coating,including composition,surface morphology,and crystalline structure,is characterized by Raman spectroscopy,scanning electron microscopy,transmission electron microscopy,and X-ray photoelectron spectroscopy,respectively.The corrosion protection performances of the composite coating are evaluated by potentiodynamic polarization tests,electrochemical impedance spectroscopy,and salt spray tests.The effect of the particle size of the N–CDs on the corrosion performance is also investigated.The results show that the corrosion performance of the N–CDs coatings are enhanced with the increase of the particle sizes.Furthermore,an obvious self-healing performance is observed on the surface of the N–CDs/PDA composite coating.These results indicate that N–CDs/PDA composite coating can improve the corrosion performance of the Mg alloy,and open a new design direction for the protective coating of metallic materials. | H.D.Zhang A.Y.Chen B.Gan H.Jiang L.J.Gu | 2022 | Journal of Magnesium and Alloys2022，10，5： | 7 |
| 12 | Autophagy-dependent removal of α-synuclein: a novel mechanism of GM1 ganglioside neuroprotection against Parkinson’s disease显示文摘GM1 ganglioside is particularly abundant in the mammalian central nervous system and has shown beneficial effects on neurodegenerative diseases.In this study,we investigated the therapeutic effect of GM1 ganglioside in experimental models of Parkinson’s disease(PD)in vivo and in vitro.Mice were injected with MPTP(30 mg·kg-1·d−1,i.p.)for 5 days,resulting in a subacute model of PD.PD mice were treated with GM1 ganglioside(25,50 mg·kg^(−1)·d^(−1),i.p.)for 2 weeks.We showed that GM1 ganglioside administration substantially improved the MPTP-induced behavioral disturbance and increased the levels of dopamine and its metabolites in the striatal tissues.In the MPP^(+)-treated SH-SY5Y cells andα-synuclein(α-Syn)A53T-overexpressing PC12(PC12^(α-Syn A53T))cells,treatment with GM1 ganglioside(40μM)significantly decreasedα-Syn accumulation and alleviated mitochondrial dysfunction and oxidative stress.We further revealed that treatment with GM1 ganglioside promoted autophagy,evidenced by the autophagosomes that appeared in the substantia nigra of PD mice as well as the changes of autophagy-related proteins(LC3-II and p62)in the MPP^(+)-treated SH-SY5Y cells.Cotreatment with the autophagy inhibitor 3-MA or bafilomycin A1 abrogated the in vivo and in vitro neuroprotective effects of GM1 ganglioside.Using GM1 ganglioside labeled with FITC fluorescent,we observed apparent colocalization of GM1-FITC andα-Syn as well as GM1-FITC and LC3 in PC12^(α-Syn A53T)cells.GM1 ganglioside significantly increased the phosphorylation of autophagy regulatory proteins ATG13 and ULK1 in doxycycline-treated PC12^(α-Syn A53T)cells and the MPP^(+)-treated SH-SY5Y cells,which was inhibited by 3-MA.Taken together,this study demonstrates that the anti-PD role of GM1 ganglioside resulted from activation of autophagy-dependentα-Syn clearance. | Yu-Lin Guo Wen-Jun Duan Dan-Hua Lu Xiao-Hui Ma Xiao-Xiao Li Zhao Li Wei Bi Hiroshi Kurihara Hai-Zhi Liu Yi-Fang Li Rong-Rong He | 2021 | Acta Pharmacologica Sinica2021，42，4： | 7 |
| 13 | Emotion processing in Parkinson's disease: a blood oxygenation level-dependent functional magnetic resonance imaging study显示文摘Parkinson's disease is a neurodegenerative disorder caused by loss of dopamine neurons in the substantia nigra pars compacta. Tremor, rigidity, and bradykinesia are the major symptoms of the disease. These motor impairments are often accompanied by affective and emotional dysfunctions which have been largely studied over the last decade. The aim of this study was to investigate emotional processing organization in the brain of patients with Parkinson's disease and to explore whether there are differences between recognition of different types of emotions in Parkinson's disease. We examined 18 patients with Parkinson's disease(8 men, 10 women) with no history of neurological or psychiatric comorbidities. All these patients underwent identical brain blood oxygenation level-dependent functional magnetic resonance imaging for emotion evaluation. Blood oxygenation level-dependent functional magnetic resonance imaging results revealed that the occipito-temporal cortices, insula, orbitofrontal cortex, basal ganglia, and parietal cortex which are involved in emotion processing, were activated during the functional control. Additionally, positive emotions activate larger volumes of the same anatomical entities than neutral and negative emotions. Results also revealed that Parkinson's disease associated with emotional disorders are increasingly recognized as disabling as classic motor symptoms. These findings help clinical physicians to recognize the emotional dysfunction of patients with Parkinson's disease. | Mohammed Benzagmout Sa?d Boujraf Badreeddine Alami Hassane Ali Amadou Halima El Hamdaoui Amine Bennani Mounir Jaafari Ismail Rammouz Mustapha Maaroufi Rabia Magoul Driss Boussaoud | 2019 | Neural Regeneration Research2019，14，4： | 6 |
| 14 | Polypropylene Separators with Robust Mussel-inspired Coatings for High Lithium-ion Battery Performances显示文摘The performances of lithium-ion batteries(LIBs)are dependent on the wettability and stability of porous separators.Musselinspired coatings seem to be useful to improve the surface wettability of commercialized polyolefin separators.However,it is still a challenge to guarantee their stability under polar electrolytes.Herein,we report a facile and versatile way to enhance the wettability and stability of polypropylene separators by constructing robust polydopamine(PDA)coatings triggered with CuSO4/H2O2.These coatings were conveniently deposited on the polypropylene separator surfaces and the PDA-coated separators exhibited the improved surface wettability and thermal stability.The electrolyte uptake increased nearly two folds from the pristine separator to the modified ones.Correspondingly,the ionic conductivity also rose from 0.82 mS·cm^-1 to 1.30 mS·cm^-1.Most importantly,the CuSO4/H2O2-triggered PDA coatings were very stable under strong polar electrolytes,endowing the cells with excellent cycle performance and enhanced C-rate capacity.Overall,the results unequivocally demonstrate that application of PDA coatings on polyolefin separator triggered by CuSO4/H2O2 is a facile and efficient method for improving the wettability and stability of separators for high LIBs performance. | Chao Zhang Hong-Qing Liang Jun-Ke Pi Guang-Peng Wu Zhi-Kang Xu | 2019 | Chinese Journal of Polymer Science2019，37，10： | 5 |
| 15 | Exogenous glutathione exerts a therapeutic effect in ischemic stroke rats by interacting with intrastriatal dopamine显示文摘We previously showed that oral administration of exogenous glutathione(GSH)exerted a direct and/or indirect therapeutic effect on ischemic stroke rats,but the underlying mechanisms remain elusive.In the current study,we conducted a quantitative proteomic analysis to explore the pathways mediating the therapeutic effect of GSH in cerebral ischemia/reperfusion(I/R)model rats.Rats were subjected to middle cerebral artery occlusion(MCAO)for 2 h followed by reperfusion.The rats were treated with GSH(250 mg/kg,ig)or levodopa(L-dopa,100 mg/kg,ig)plus carbidopa(10 mg/kg,ig).Neurologic deficits were assessed,and the rats were sacrificed at 24 h after cerebral I/R surgery to measure brain infarct sizes.We conducted a proteomic analysis of the lesion side striatum samples and found that tyrosine metabolism and dopaminergic synapse were involved in the occurrence of cerebral stroke and the therapeutic effect of GSH.Western blot assay revealed that tyrosine hydroxylase(TH)mediated the occurrence of I/R-induced ischemic stroke and the therapeutic effect of GSH.We analyzed the regulation of GSH on endogenous small molecule metabolites and showed that exogenous GSH had the most significant effect on intrastriatal dopamine(DA)in I/R model rats by promoting its synthesis and inhibiting its degradation.To further explore whether DA-related alterations were potential targets of GSH,we investigated the therapeutic effect of DA accumulation on ischemic brain injury.The combined administration of the precursor drugs of DA(L-dopa and carbidopa)significantly ameliorated neurological deficits,reduced infarct size,and oxidative stress,and decreased pro-inflammatory cytokines levels in the striatum of I/R injury rats.More interestingly,exogenous L-dopa/carbidopa could also greatly enhance the exposure of intracerebral GSH by upregulating GSH synthetases and enhancing homocysteine(HCY)levels in the striatum.Thus,administration of exogenous GSH exerts a therapeutic effect on ischemic stroke by increasing intrastriatal DA,and the accumulated DA can,in turn,enhance the exposure of GSH and its related substances,thus promoting the therapeutic effect of GSH. | He Wang Yi-sha Du Wen-shuo Xu Chang-jian Li Hong Sun Kang-rui Hu Yuan-zhuo Hu Teng-jie Yu Hui-min Guo Lin Xie Guang-ji Wang Yan Liang | 2022 | Acta Pharmacologica Sinica2022，43，3： | 5 |
| 16 | Enhancement of Aggression Induced by Isolation Rearing is Associated with a Lack of Central Serotonin显示文摘Isolation rearing(IR) enhances aggressive behavior, and the central serotonin(5-hydroxytryptamine,5-HT) system has been linked to IR-induced aggression.However, whether the alteration of central serotonin is the cause or consequence of enhanced aggression is still unknown. In the present study, using mice deficient in central serotonin Tph2-/-and Lmx1 b-/-, we examined the association between central serotonin and aggression with or without social isolation. We demonstrated that central serotonergic neurons are critical for the enhanced aggression after IR. 5-HT depletion in wild-type mice increased aggression. On the other hand, application of 5-HT in Lmx1 b-/-mice inhibited the enhancement of aggression under social isolation conditions. Dopamine was downregulated in Lmx1 b-/-mice. Similar to 5-HT, L-DOPA decreased aggression in Lmx1 b-/-mice. Our results linkthe serotoninergic system directly to aggression and this may have clinical implications for aggression-related human conditions. | Yiqiong Liu Yunong Sun Xiaoyan Zhao Ji-Young Kim Lu Luo Qian Wang Xiaolu Meng Yonghui Li Nan Sui Zhou-Feng Chen Chuxiong Pan Liang Li Yan Zhang | 2019 | Neuroscience Bulletin2019，35，5： | 5 |
| 17 | Effect of dopamine on bone morphogenesis protein-2 expression in human retinal pigment epithelium显示文摘AIM: To investigate the effect of dopamine on bone morphogenesis protein-2(BMP-2) expression in retinal pigment epithelium(RPE) cells in vitro.METHODS: ARPE-19 cells as a human RPE cell line were cultured with dopamine for different times(2, 4, 6, 8, 12, 16 and 24h) or with different concentrations(0.1, 1, 2, 5, 10, 20, and 100 μg/mL) in vitro. BMP-2 m RNA expression level in ARPE-19 cells was analyzed with real-time polymerase chain reaction(PCR) analysis and BMP-2 protein level was measured with Western blot analysis. The active form of BMP-2 in the culture medium was measured with enzymelinked immunosorbent assay(ELISA).RESULTS: The expression level of BMP-2 increased significantly cultured with 20 μg/mL dopamine, at different time points(P<0.05). BMP-2 m RNA level peaked 2h and the protein level peaked at 6 and 8h after treatment. The concentrations of secreted BMP-2 elevated at 12 h and peaked at 24h(P<0.05) in a time-dependent manner. Treated with 100 μg/mL dopamine for 6h, the expression levels of BMP-2 m RNA and protein in ARPE-19 cells were enhanced significantly compared to that in the untreated cells(P<0.05). And secreted BMP-2 protein in the cell culture supernatant was also increased(P<0.05).CONCLUSION: Dopamine up-regulate BMP-2 expression in RPE cells, and this may be associated with its inhibitive effect on myopia development. | Hong-Hui Li Yan-Li Sun Dong-Mei Cui Juan Wu Jun-Wen Zeng | 2017 | International Journal of Ophthalmology(English edition)2017，10，9： | 5 |
| 18 | Dopamine: an immune transmitter显示文摘The dopaminergic system controls several vital central nervous system functions, including the control of movement, reward behaviors and cognition. Alterations of dopaminergic signaling are involved in the pathogenesis of neurodegenerative and psychiatric disorders, in particular Parkinson’s disease, which are associated with a subtle and chronic inflammatory response. A substantial body of evidence has demonstrated the non-neuronal expression of dopamine, its receptors and of the machinery that governs synthesis, secretion and storage of dopamine across several immune cell types. This review aims to summarize current knowledge on the role and expression of dopamine in immune cells. One of the goals is to decipher the complex mechanisms through which these cell types respond to dopamine, in order to address the impact this has on neurodegenerative and psychiatric pathologies such as Parkinson’s disease. A further aim is to illustrate the gaps in our understanding of the physiological roles of dopamine to encourage more targeted research focused on understanding the consequences of aberrant dopamine production on immune regulation. These highlights may prompt scientists in the field to consider alternative functions of this important neurotransmitter when targeting neuroinflammatory/neurodegenerative pathologies. | Sarah Thomas Broome Krystal Louangaphay Kevin AKeay Gian Marco Leggio Giuseppe Musumeci Alessandro Castorina | 2020 | Neural Regeneration Research2020，15，12： | 5 |
| 19 | Parkinson’s disease and diabetes mellitus: common mechanisms and treatment repurposing显示文摘In the last decade,attention has become greater to the relationship between neurodegeneration and abnormal insulin signaling in the central nervous system,as insulin in the brain is implicated in neuronal survival,plasticity,oxidative stress and neuroinflammation.Diabetes mellitus and Parkinson’s disease are both aging-associated diseases that are turning into epidemics worldwide.Diabetes mellitus and insulin resistance not only increase the possibility of developing Parkinson’s disease but can also determine the prognosis and progression of Parkinsonian symptoms.Today,there are no available curative or disease modifying treatments for Parkinson’s disease,but the role of insulin and antidiabetic medications in neurodegeneration opens a door to treatment repurposing to fight against Parkinson’s disease,both in diabetic and nondiabetic Parkinsonian patients.Furthermore,it is essential to comprehend how a frequent and treatable disease such as diabetes can influence the progression of neurodegeneration in a challenging disease such as Parkinson’s disease.Here,we review the present evidence on the connection between Parkinson’s disease and diabetes and the consequential implications of the existing antidiabetic molecules in the severity and development of Parkinsonism,with a particular focus on glucagon-like peptide-1 receptor agonists. | Carmen M.Labandeira Arturo Fraga-Bau David Arias Ron Elena Alvarez-Rodriguez Pablo Vicente-Alba Javier Lago-Garma Ana I.Rodriguez-Perez | 2022 | Neural Regeneration Research2022，17，8： | 5 |
| 20 | Smoking in schizophrenic patients:A critique of the selfmedication hypothesis显示文摘A common remark among laypeople, and notably also among mental health workers, is that individuals with mental illnesses use drugs as self-medication to allay clinical symptoms and the side effects of drug treatments. Roots of the self-medication concept in psychiatry date back at least to the 1980 s. Observations that rates of smokers in schizophrenic patients are multiple times the rates for regular smoking in the general population, as well as those with other disorders, proved particularly tempting for a self-medication explanation. Additional evidence came from experiments with animal models exposed to nicotine and the identification of neurobiological mechanisms suggesting self-medication with smoking is a plausible idea. More recently, results from studies comparing smoking and non-smoking schizophrenic patients have led to the questioning of the self-medication hypothesis. Closer examination of the literature points to the possibility that smoking is less beneficial on schizophrenic symptomology than generally assumed while clearly increasing the risk of cancer and other smoking-related diseases responsible for early mortality. It is a good time to examine the evidence for the self-medication concept as it relates to smoking. Our approach is to focus on data addressing direct or implied predictions of the hypothesis in schizophrenic smokers. | Francesca Manzella Susan E Maloney George T Taylor | 2015 | World Journal of Psychiatry2015，5，1： | 4 |
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