Paeoniflorin inhibits epithelial mesenchymal transformation and oxidative damage of lens epithelial cells in diabetic cataract via sirtuin 1 upregulation.

Paeoniflorin (Pae) has been reported to serve an important role in complications associated with diabetes. To the best of our knowledge, the role of Pae in diabetic cataracts has not yet been reported. Human lens epithelial SRA01/04 cells were induced by high glucose (HG) and subsequently treated with Pae. Cell viability was detected using the MTT assay. Moreover, LDH levels were detected. Immunofluorescence (IF) and Western blotting were used to determine the protein expression levels of N-cadherin and E-cadherin. ELISA was performed to determine oxidative stress-related indicator levels. TUNEL and Western blotting detected the apoptotic rate. The mRNA and protein expression levels of sirtuin 1 (SIRT1) in SRA01/04 cells were measured via reverse transcription-quantitative PCR and Western blotting, respectively. Subsequently, cell transfection techniques were used to inhibit the expression of SIRT1 in cells. MTT, ELISA, IF, Western blotting and TUNEL assays were used to investigate the mechanisms of epithelial-mesenchymal transition (EMT) and oxidative damage with Pae in the diabetic cataract. Pae significantly increased cell viability and possibly inhibit the EMT and oxidative damage of SRA01/04 cells induced by HG. Pae was demonstrated to upregulate SIRT1 expression levels. The results therefore suggested that the downregulation of SIRT1 reversed the protective effect of Pae on EMT and oxidative damage in SRA01/04 cells induced by HG. In conclusion, Pae may inhibit EMT of lens epithelial cells and reduce oxidative damage in diabetic cataracts via the upregulation of SIRT1.