Research Paper Volume 13, Issue 8 pp 11774—11785

Inhibition of sestrin 1 alleviates polycystic ovary syndrome by decreasing autophagy

Sestrin 1 knockdown promoted apoptosis in KGN cells by inhibiting autophagy. (A) Western blots were performed to determine the levels of apoptosis associated proteins, including Bax, cleaved caspase 3, bcl-2, and p53. β-actin was used as an internal control. (B–E) Quantitative analysis of Bax, cleaved caspase 3, Bcl-2, and p53 expression in KGN cells. (F) Cell apoptosis was detected using annexin V/PI staining followed by flow cytometry. (G) Cell apoptosis rates were quantified. **P ##P

Figure 6. Sestrin 1 knockdown promoted apoptosis in KGN cells by inhibiting autophagy. (A) Western blots were performed to determine the levels of apoptosis associated proteins, including Bax, cleaved caspase 3, bcl-2, and p53. β-actin was used as an internal control. (BE) Quantitative analysis of Bax, cleaved caspase 3, Bcl-2, and p53 expression in KGN cells. (F) Cell apoptosis was detected using annexin V/PI staining followed by flow cytometry. (G) Cell apoptosis rates were quantified. **P < 0.01 compared to the blank control. ##P < 0.01 compared to the sestrin 1 siRNA2 group.