- Author:
Meng-Jie HAN
1
;
Juan WANG
1
;
Guo-Xiang LIU
1
;
Ting LI
1
;
Lu-Wei ZHOU
1
;
Xu CHEN
1
Author Information
- Publication Type:Journal Article
- Keywords: H2 02 ± PI3 K/Akt; islet MIN6 cells; MK2206; mogrosicle V; oxidative damage
- From: Chinese Pharmacological Bulletin 2022;38(9):1363-1368
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the protective effect of mogroside V on hydrogen peroxide ( H,02 )-induced oxidative stress response in mouse islet (3 cells MIN6 and the relation of its mechanism to PI3K/Akt signa¬ling pathway.Methods MIN6 cells were treated with 500 (jimol • L_1 H,(), after mogroside V,and cell via¬bility was detected by MTT.The release of reactive ox¬ygen species ( ROS) and apoptotic percentage of MIN6 cells were determined by flow cytometry.The expres¬sions of apoptosis-related factor Bel-2 , proliferation-re¬lated factor PCNA, protein Akt and p-Akt were deter¬mined by Western blot.Results H,02 restrained the proliferation of MIN6 cells obviously, induced ROS pro¬duction and apoptosis, and reduced the expression of Bel-2 and PCN A.The expressions of protein Akt and p-Akt decreased.After treatment of mogroside V , the release of ROS decreased, and the apoptosis of MIN6 cells was inhibited.The expression levels of apoptosis- related protein Bcl-2 and proliferation-related protein PCN A were reversed.The expressions of protein Akt and P-Akt increased.The viability of MIN6 cells in¬duced by H,0, increased.In addition, mogroside V partly reversed the apoptosis induction and ROS pro¬duction of Akt inhibitor MK2206 (5 jjimol • L"1 ) on MIN6 cells.Conclusions Mogroside V has protec¬tive effect on H202-induced oxidative damage in MIN6 cells and its mechanism is related to PI3K/Akt signa¬ling pathway.