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Effect of metformin on cell senescence through IGF-1/PI3K/Akt signaling pathway |
HOU Yuli FU Jingxuan WANG Peichang |
Department of Laboratory, Xuanwu Hospital, Capital Medical University, Beijing 100053, China |
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Abstract Objective To explore the effect of metformin (Met) on cell senescence through IGF-1/PI3K/Akt signaling pathway. Methods 2BS cells were selected and divided into four groups, namely control (NC) group, insulin-like growth factor-1 (IGF-1) group, Met group, Met+ IGF-1 group. After drug treatment, SA-β-Gal staining was performed to detect cell senescence, CCK8 test was used to detect cell proliferation ability, EdU test was performed to detect DNA synthesis ability, and Western blot was used to detect the protein expression of PI3K, p-PI3K, Akt, and p-Akt in each group. Results The positive rate of SA-β-Gal staining in each group was compared, and the difference was statistically significant (P < 0.05). The positive rate of SA-β-Gal staining in Met+IGF-1 group was lower than that in IGF-1 group, and the difference was highly statistically significant (P < 0.01). At the same time point, the OD450 value of the Met+IGF-1 group was higher than that of the IGF-1 group, and the difference was statistically significant (P < 0.05). The staining results at 370 nm after EdU staining showed that the OD370 value of each group was compared with statistical significance (P < 0.05); the OD370 value of the Met+IGF-1 group was higher than that of the IGF-1 group, and the difference was statistically significant (P < 0.05). The expressions of p-PI3K and p-Akt protein in Met group were lower than those in other groups, and the differences were statistically significant (P < 0.05). The expression of p-PI3K and p-Akt protein in IGF-1 group were higher than those in other groups, and the differences were statistically significant (P < 0.05). The expressions of p-PI3K and p-Akt protein in Met+IGF-1 group were lower than those in IGF-1 group, and the differences were statistically significant (P < 0.05). Conclusion Metformin can delay cell senescence by inhibiting IGF-1/PI3K/Akt signaling pathway.
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