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| Protective effect of ginsenoside Rb1 on regulating endoplasmic reticulum stress in important organs of septic mice |
| HUANG Min1 TAO Xingyu2 JIA Baohui3,4 YANG Shaolong5 XU Chunfeng1 |
1.Department of Geriatric Medicine, the Third Affiliated Hospital of Nanchang University, Jiangxi Province, Nangchang 330000, China;
2.Department of Critical Care Medicine, the Fourth Affiliated Hospital of Nanchang University, Jiangxi Province, Nangchang 330003, China;
3.He′nan Provincial Research Center of Natural Medicine Extraction & Medical Technology Application Engineering, He′nan Province, Zhengzhou 451460, China; 4.the Key Laboratory of Severe Infection, Trauma and Repair in Zhengzhou City, He′nan Province, Zhengzhou 450007, China;
5.Department of Pathology, Zhengzhou Railway Vocational & Technical College, He′nan Province, Zhengzhou 450052, China |
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Abstract Objective To observe the effects of ginsenoside Rb1 on endoplasmic reticulum stress in important organs of sepsis mice, and to explore the molecular mechanism of the protective effect of ginsenoside Rb1 on sepsis. Methods The sepsis model was reproduced by cecal ligation and perforation (CLP). Sixty adult (4-6 weeks old) C57BL/6 female mice were randomly divided into the normal group, the false CLP group, the ginsenoside group and the CLP group, with 15 mice in each group. The general state of the mice was observed after successful model preparation. The general state of the mice was observed. The mice were sacrificed 24 h after the operation, and the cardiac muscle and lung tissue were taken for pathological examination. The expressions of glucose regulated protein 78 kD (GRP78) and caspase-12 proteins in cardiac muscle and lung tissue were detected by Western blotting. Results Compared with the CLP group, the general status of mice in the ginsenoside group was significantly improved. Compared with the CLP group, the pulmonary alveoli tissue structure of the ginsenoside group was relatively clear and complete, inflammatory cell infiltration was reduced, and pulmonary alveoli size was uniform. In the ginsenoside group, there were fewer inflammatory cells, striations and necrotic cells in the cardiac muscle tissue. Compared with the CLP group, GRP78 and caspase-12 protein expression levels in cardiac muscle and lung tissue of the ginsenoside group were significantly decreased, with highly statistically significant differences (all P ＜ 0.01). Conclusion Ginsenoside Rb1 can reduce the severity of infection in sepsis mice, and has a protective effect on the injury of heart and lung tissue in mice. Its mechanism may be related to the inhibition of endoplasmic reticulum stress overexpression by ginsenoside Rb1.
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