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| 1 | Mogroside V inhibits LPS-induced COX-2 expression/ROS production and overexpression of HO-1 by blocking phosphorylation of AKT1 in RAW264.7 cells显示文摘Momordica grosvenori is a valuable edible plant with medicinal purposes, and it is widely used in medicated diets and traditional Chinese medicine in Asia. Mogroside V (MV), the main bioactive component from M. grosvenori, is comm only used as a natural sweetener. M. grosvenori extracts have been reported to exert potent anti-inflammatory property, however the underlying molecular mechanism still remains unknown. In the present study, the biological effect of MV in inflammation was investigated in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The ELISA and western blot analysis results showed that MV significantly inhibited LPS-induced prostaglandin E2 (PGE2) production and cyclooxygenase-2 (COX-2) expression. MV markedly decreased the phosphorylation of IxB-a, increased IkB-oc, and reduced nuclear p-65 and C/EBP6. Furthermore, MV attenuated LPS-induced phosphorylation of MAPKs and AKT1, and only the phosphorylation status of AKT1 was found to be consistent with the expression trend of COX-2. Moreover, MV reduced ROS level and restored overexpressed HO-1 and AP-1 to basal level, which can be markedly reversed by AKT1 inhibitor LY294002. These results revealed that AKT1 plays a key role in LPS-induced COX-2 expression, and acts as a mediator to keep the redox balance in LPS-stimulated RAW264.7 cells. MV exerts anti-inflammatory property by blocking AKT1-mediated NF-kB and C/EBP6 activation, ROS generation and AP-1/ HO-1 expression. Therefore, the present study indicated that MV has a significant chemopreventive effect on the inflammatory lesions and suggested that AKT1 is a potential specific target of MV for relieving inflammation. | Yong Li Luyan Zou Tao Li Dengni Lai Yanyang Wu Si Qin | 2019 | Acta Biochimica et Biophysica Sinica2019，51，4： | 14 |
| 2 | Delphinidin-induced autophagy protects pancreatic β cells against apoptosis resulting from high-glucose stress via AMPK signaling pathway显示文摘Hyperglycemia,a diagnostic characteristic of diabetes mellitus,is detrimental to pancreatic 0 cells.Delphinidin,a member of the anthocyanin family,inhibits glucose absorption,increases glucagonlike peptide(GLP-1)secretion,and improves insulin secretion in diabetes.However,whether delphinidin plays a protective role in pancreatic p-cell mass and function is not clear.In this study,delphinidin was found to decrease the high-glucose-induced apoptosis of RIN-m5F pancreatic β cells.In addition,delphinidin induced autophagy in RIN-m5F cells under the normal and highglucose conditions,while 3-methyladenine(3-MA)inhibition of autophagy significantly diminished the protective role of delphinidin against high-glucose-induced apoptosis of pancreatic β cells.Delphinidin also decreased the level of cleaved caspase 3 and increased the phosphorylation level of AMP-activated protein kinase a(AMPKa)Thr172.Compound C,an AMPK inhibitor,was found to decrease the ratio of LC3-II/LC3-I,and the apoptotic rate of high-glucose-injured cells was in creased after treatme nt with delphinidin,in dicating that delphinidi n attenuated the n egative effects of high-glucose stress to cells.In con elusion,our data dem on strate that delphi nidin protects pancreatic B cells against high-glucose-induced injury by autophagy regulation via the AMPK signaling pathway.These findings might shed light on the underlying mechanisms of diabetes and help improve the prevention and therapy of this common disease. | Dengni Lai Mingyong Huang Lingyan Zhao Yan Tian Yong Li Dongpo Liu Yanyang Wu Fangming Deng | 2019 | Acta Biochimica et Biophysica Sinica2019，51，12： | 3 |
| 3 | Vitamin B3 inhibits apoptosis and promotes autophagy of isletβcells under high glucose stress显示文摘Background:Hyperglycemia is a typical symptom of diabetes.High glucose induces apoptosis of isletβcells.While autophagy functions in cytoprotection and autophagic cell death.The interaction between autophagy and apoptosis is important in the modulation of the function of isletβcells.Vitamin B3 can induce autophagy and inhibit isletβapoptosis.Method:The mechanism of vitamin B3-mediated protective effect on the function of isletβcells was explored by the method of western blot,immunofluorescence and flow cytometry.Results:In the present study,high glucose stress increased the apoptosis rate,while vitamin B3 reduced the apoptosis rate.The effect of vitamin B3 on autophagy flux under normal and high glucose stress was also investigated.Vitamin B3 increased the number of autophagosomes and increased the light chain(LC)3-II/LC3-I ratio.In contrast,vitamin B3 decreased sequestosome 1(SQSTM1)/p62 protein expression and inhibited the phosphorylation of mammalian ribosomal protein S6 kinaseβ-1(p70S6K/S6K1),which was a substrate of mammalian target of rapamycin(mTOR)under normal and high glucose stress.To further verify the protective effect of vitamin B3 on apoptosis,we treated isletβcell RIN-m5F with autophagy inhibitor 3-methyladenine(3-MA).Vitamin B3 decreased the apoptosis rate under high glucose stress,while the inhibition of apoptosis by vitamin B3 was blocked after adding 3-MA.Conclusion:Our data suggested that vitamin B3 reduced the apoptosis rate ofβcells,possibly through inducing autophagy under high glucose stress. | YU ZHANG XI’AN ZHOU CHUNYAN ZHANG DENGNI LAI DONGBO LIU YANYANG WU | 2023 | BIOCELL2023，47，4： | 1 |
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