Fig 2: Underlying mechanisms of CHP and CHL exerts and their anti-senescent activity in SH-SY5Y cells. (a) In hyperglycemia, hyperphosphorylation of Rb induced by high glucose and cyclin D1 caused cell cycle arrest at G1. Hyperphosphorylated Rb failed to assemble with E2F. Furthermore, pcdc2 was an inactive form that caused cell cycle arrest. (b) Both extracts could reduce high glucose level. Low cellular glucose significantly increased GAPDH phosphorylation via AMP-activated protein kinase (AMPK), triggering SIRT1 activation. This mechanism induced the cell cycle progression by decreasing Rb and cdc2 phosphorylation. High expression of proteins (); Low expression of proteins (); Hyperphosphorylation of proteins (); Hypophosphorylation of proteins ().

Fig 3: Correlation of between SIRT1 and BCL6. (a) Correlation analysis between SIRT1 and BCL6 in human endometrium with endometriosis. (b) Immunoprecipitation (IP) analysis between SIRT1 and BCL6 in Ishikawa cells and Human endometrium with endometriosis. Representative blots have been cropped to reduce unnecessary area. Full-length blots are presented in Supplementary Fig. S4. (c) Co-localization of SIRT1 and BCL6 in the human endometrium without and with endometriosis by immunofluorescence analysis.

Fig 4: Role of the SIRT1/Nrf2/GPx4 signaling pathway in ferroptosis. (A) Western blot analysis of SIRT1, Nrf2, and GPx4 expression indicated upregulation of SIRT1 and Nrf2 and downregulation of GPx4 after HIBI induction. SIRT1, Nrf2, and GPx4 expression was upregulated after Res administration (n = 5 per group). (B) Quantification of SIRT1. (C,D) Quantification of (C) Nrf2 and (D) GPx4. Data represent the mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001 vs. the Sham group; ##p < 0.01 vs. the HIBI group. HIBI, hypoxic–ischemic brain injury; GPx4, glutathione peroxidase 4; Fer‐1, ferrostatin‐1; SIRT1, silent information regulator factor 2‐related enzyme 1; Nrf2, nuclear factor erythroid‐2‐related factor 2; Res, resveratrol; GAPDH, glyceraldehyde 3‐phosphate dehydrogenase; CA1, cornu ammonis 1.

Fig 5: APN conferred protective effects through SIRT1- PINK1-dependent mitophagy in PMVECs subjected to diabetic IR injury. A Mitochondrial membrane potential visualized by JC-1(scale bars, 20 μm). B The amount of ROS in PMVECs was determined by MitoSOX (scale bars, 20 μm). C Quantification of JC-1 fluorescence intensity (red/green florescent area) (mean ± SD). D Quantification of MitoSOX fluorescence intensity (red) (mean ± SD). E Mitochondrial ultrastructure. Mitochondria (red arrows) and mitophagosome (white arrows) in PMVECs were imaged with transmission electron microscopy (scale bars, 2 μm). F Flameng score (medians, interquartile range). G Cell apoptosis was determined by flow cytometry in rat PMVECs (medians, interquartile range). HF high fat, HG high glucose, SIR simulated ischemia–reperfusion. (ccP < 0.05 versus the HG/HG + SIR group, ddP < 0.05 versus the HG/HG + SIR + A group)