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冰片对缺氧/复氧H9c2细胞凋亡及大鼠心肌缺血再灌注损伤的影响

Effects of borneol on apoptosis of hypoxia/reoxygenation H9c2 cells and myocardial ischemia-reperfusion injury rats.

作者信息

Zhang Hui, Dong Junfang, Zhang Jianwu, Chen Hongxue, Liu Ting, Gan Ruixue, Wen Jing, Li Yangyou

机构信息

North Sichuan Medical College - Department of Pharmacy - Nanchong, Sichuan - China.

North Sichuan Medical College - Animal Experimental Center - Nanchong, Sichuan - China.

出版信息

Acta Cir Bras. 2025 Mar 14;40:e402225. doi: 10.1590/acb402225. eCollection 2025.

Abstract

PURPOSE

To explore the protective effects of borneol in myocardial ischemia-reperfusion injury (MIRI) and the mechanism of apoptosis.

METHODS

Cell viability was detected by CCK-8. The total superoxide dismutase (T-SOD) and lactate dehydrogenase (LDH) leakage of cells were tested by biochemical assay kit. Detection of apoptosis was by flow cytometry. Serum levels of creatine kinase isoenzyme MB (CK-MB), LDH, and cardiac troponin I (cTnI) were detected by enzyme-linked immunosorbent assay. Myocardial infarction area and pathological changes were observed via 2,3,5-triphenyltetrazolium chloride (TTC) staining and hematoxylin and eosin staining. The expressions of apoptosis-related proteins in cells and myocardial tissues were detected by Western blot.

RESULTS

H9c2 cell viability was significantly increased by pretreatment with 16 and 32 μg/mL of borneol. Borneol pretreatment significantly increased the T-SOD levels and reduced LDH leakage and apoptosis. In MIRI rats, borneol pretreatment significantly reduced serum levels of CK-MB, LDH and cTnI, decreased myocardial infarction area, and improved myocardial injury in different degree. Western blot results showed that borneol pretreatment significantly reduced the expression of Bcl-2-associated X protein (Bax) and Cysteine-aspartate protease-3 (Caspase-3) in cells and myocardial tissues of rats.

CONCLUSION

Borneol can protect myocardial injury cells and mitigate MIRI by inhibiting cardiomyocyte apoptosis.

摘要

目的

探讨冰片对心肌缺血再灌注损伤(MIRI)的保护作用及细胞凋亡机制。

方法

采用CCK-8法检测细胞活力。用生化检测试剂盒检测细胞总超氧化物歧化酶(T-SOD)和乳酸脱氢酶(LDH)漏出率。通过流式细胞术检测细胞凋亡。采用酶联免疫吸附测定法检测血清肌酸激酶同工酶MB(CK-MB)、LDH和心肌肌钙蛋白I(cTnI)水平。通过2,3,5-三苯基氯化四氮唑(TTC)染色及苏木精-伊红染色观察心肌梗死面积及病理变化。采用蛋白质免疫印迹法检测细胞及心肌组织中凋亡相关蛋白的表达。

结果

16和32μg/mL冰片预处理可显著提高H9c2细胞活力。冰片预处理可显著提高T-SOD水平,降低LDH漏出率及细胞凋亡。在MIRI大鼠中,冰片预处理可显著降低血清CK-MB、LDH和cTnI水平,减小心肌梗死面积,并不同程度改善心肌损伤。蛋白质免疫印迹结果显示,冰片预处理可显著降低大鼠细胞及心肌组织中Bcl-2相关X蛋白(Bax)和半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的表达。

结论

冰片可通过抑制心肌细胞凋亡保护心肌损伤细胞,减轻MIRI。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49d9/11908740/dcaad0f6a9aa/1678-2674-acb-40-e402225-gf01.jpg

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