PMID- 34306208 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20240402 IS - 1792-1015 (Electronic) IS - 1792-0981 (Print) IS - 1792-0981 (Linking) VI - 22 IP - 3 DP - 2021 Sep TI - Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress. PG - 944 LID - 10.3892/etm.2021.10376 [doi] LID - 944 AB - Diabetic cardiomyopathy is a common complication of diabetes, in which endoplasmic reticulum stress (ERS) serves an important role. Rutin can treat the myocardial dysfunction of diabetic rats. However, to the best of our knowledge, studies on the effects of Rutin on myocardial injury caused by diabetes from the perspective of ERS have not previously been reported. In the present study, the role of rutin in the regulation of ERS in myocardial injury was assessed. Different high glucose concentrations were used to treat H9C2 myoblast cells to establish a myocardial damage model. A cell counting kit-8 assay was used to determine cell viability. A lactate dehydrogenase kit was used to detect cytotoxicity. Apoptosis levels were determined using a TUNEL assay. Western blotting was used to determine the expression levels of apoptosis-related proteins and ERS-related proteins, including heat shock protein A family member 5, inositol-requiring enzyme-1alpha, X-box binding protein 1, activating transcription factor 6, C/EBP-homologous protein (CHOP), cleaved caspase-12 and caspase-12. The anti-apoptotic and anti-ERS effects of Rutin on H9C2 cardiac cells induced by high glucose were examined after the administration of the ERS activator thapsigargin (TG). The results indicated that rutin could dose-dependently inhibit the level of apoptosis and ERS induced by high glucose in H9C2 cells. After administration of the ERS activator TG, it was demonstrated that TG could reverse the anti-apoptotic and anti-ERS effects of rutin on H9C2 cells stimulated with high glucose. Collectively, the present results suggested that rutin may alleviate cardiomyocyte model cell injury induced by high glucose through the inhibition of apoptosis and ERS. CI - Copyright: (c) Wang et al. FAU - Wang, Jing AU - Wang J AD - Department of Cardiology, Tianjin Union Medical Center, Tianjin 300121, P.R. China. FAU - Wang, Ru AU - Wang R AD - Department of Cardiology, Tianjin Union Medical Center, Tianjin 300121, P.R. China. FAU - Li, Jiali AU - Li J AD - Department of Cardiology, Tianjin Union Medical Center, Tianjin 300121, P.R. China. FAU - Yao, Zhuhua AU - Yao Z AD - Department of Cardiology, Tianjin Union Medical Center, Tianjin 300121, P.R. China. LA - eng PT - Journal Article DEP - 20210701 PL - Greece TA - Exp Ther Med JT - Experimental and therapeutic medicine JID - 101531947 PMC - PMC8281503 OTO - NOTNLM OT - apoptosis OT - cardiomyocyte injury OT - diabetic cardiomyopathy OT - endoplasmic reticulum stress OT - rutin COIS- The authors declare that they have no competing interests. EDAT- 2021/07/27 06:00 MHDA- 2021/07/27 06:01 PMCR- 2021/07/01 CRDT- 2021/07/26 06:26 PHST- 2020/10/23 00:00 [received] PHST- 2021/03/18 00:00 [accepted] PHST- 2021/07/26 06:26 [entrez] PHST- 2021/07/27 06:00 [pubmed] PHST- 2021/07/27 06:01 [medline] PHST- 2021/07/01 00:00 [pmc-release] AID - ETM-0-0-10376 [pii] AID - 10.3892/etm.2021.10376 [doi] PST - ppublish SO - Exp Ther Med. 2021 Sep;22(3):944. doi: 10.3892/etm.2021.10376. Epub 2021 Jul 1.