TY - JOUR AB - Penehyclidine hydrochloride (PHC) suppresses renal ischemia and reperfusion (I/R) injury (IRI); however, the underlying mechanism of action that achieves this function remains largely unknown. The present study aimed to investigate the potential role of autophagy in PHC‑induced suppression of renal IRI, as well as the involvement of cell proliferation and apoptosis. A rat IRI model and a cellular hypoxia/oxygenation (H/R) model were established; PHC, 3‑methyladenine (3‑MA) and rapamycin (Rapa) were administered to the IRI model rats prior to I/R induction and to H/R cells following reperfusion. Serum creatinine was measured using a biochemistry analyzer, whereas aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) expression levels were detected using ELISA kits. Renal tissue injury was evaluated by histological examination. In addition, microtubule‑associated protein light chain 3B (LC3B) expression, autophagosome formation, cell proliferation and apoptosis were detected in the cellular H/R model. The results demonstrated that I/R induced renal injury in IRI model rats, upregulated serum creatinine, ALAT and ASAT expression levels, and increased autophagic processes. In contrast, pretreatment with PHC or Rapa significantly prevented these I/R‑induced changes, whereas the administration of 3‑MA enhanced I/R‑induced injuries through suppressing autophagy. PHC and Rapa increased LC3B and Beclin‑1 expression levels, but decreased sequestome 1 (p62) expression in the cellular H/R model, whereas 3‑MA prevented these PHC‑induced changes. PHC and Rapa promoted proliferation and autophagy in the cellular H/R model; these effects were accompanied by increased expression levels of LC3B and Beclin‑1, and reduced p62 expression levels, whereas these levels were inhibited by 3‑MA. Furthermore, PHC and Rapa inhibited apoptosis in the cellular H/R model through increasing Bcl‑2 expression levels, and suppressing Bax and caspase‑3 expression levels; the opposite effect was induced by 3‑MA. In conclusion, PHC suppressed renal IRI through the induction of autophagy, which in turn promoted proliferation and suppressed apoptosis in renal cells. AD - Department of Anesthesiology, Jinshan Branch Hospital of Shanghai Sixth People's Hospital, Shanghai 201599, P.R. China Department of Anesthesiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China AU - Kang,Yuqing AU - Li,Yuebing AU - Wen,Heng AU - Zhu,Junfeng AU - Zheng,Jiangbo AU - Feng,Zhaoming DA - 2020/05/01 DO - 10.3892/mmr.2020.11024 EP - 2192 IS - 5 JO - Mol Med Rep KW - penehyclidine hydrochloride renal ischemia and reperfusion injury autophagy proliferation apoptosis PY - 2020 SN - 1791-2997 1791-3004 SP - 2182 ST - Prevention of renal ischemia and reperfusion injury by penehyclidine hydrochloride through autophagy activation T2 - Molecular Medicine Reports TI - Prevention of renal ischemia and reperfusion injury by penehyclidine hydrochloride through autophagy activation UR - https://doi.org/10.3892/mmr.2020.11024 VL - 21 ER -