Objective

The objective was to investigate the anti-inflammatory effects of salidroside through the PI3K/Akt signaling pathway and its protective effects on acute hypoxia-induced myocardial injury in rats.

Methods

A total of 24 healthy Sprague-Dawley male rats were selected as the experimental subjects. All rats were divided into 4 groups by using the random number table method, with 6 rats in each group. The groups included the normal control group, the salidroside group, the hypobaric hypoxia group, and the hypobaric hypoxia + salidroside group. Rats in the salidroside group were fed in the original animal laboratory and were intragastrically administered with salidroside every morning at a dosage of 35 mg/kg. Rats in the normal control group were intragastrically administered with an equal dosage of saline. Rats in the hypobaric hypoxia + salidroside group were intragastrically administered with salidroside every morning at a dosage of 35 mg/kg, who were fed in the hypoxic experiment module for animals. The altitude was increased to 4000 m, and the rats were kept in the module for 24 h. Rats in the hypobaric hypoxia group were intragastrically administered with an equal dosage of saline in the same environment, and the altitude was increased to 4000 m after administration. Parameters of blood gas analysis, histopathological changes in cardiac tissues, cardiac indexes, and inflammatory factors IL-6 and TNF-α levels of rats in groups were compared.

Results

1. The cardiac indexes of rats in groups were compared. The differences between the hypobaric hypoxia group and the hypobaric hypoxia + salidroside group were statistically significant (P < 0.05). 2. The results of blood gas analysis of rats in groups were compared. The differences between the hypobaric hypoxia group and the hypobaric hypoxia + salidroside group were significantly different (P < 0.05). 3. In the hypobaric hypoxia group, the myocardial cells of rats were arranged disorderly and shaped differently, with cases such as edema, degeneration, necrosis, nucleus pyknosis, and massive infiltration of inflammatory cells. In the hypobaric hypoxia + salidroside group, the above-mentioned pathological changes in myocardial cells were relieved. 4. Compared with the hypobaric hypoxia group, in the hypobaric hypoxia + salidroside group, the concentrations of IL-6 and TNF-α in rats decreased apparently, and the differences were statistically significant (P < 0.05).

Conclusion

Salidroside had the repairing and protective effects on the hypobaric hypoxia-induced myocardial injuries in rats. The application of salidroside could reduce the inflammatory responses of rats with hypobaric hypoxia-induced myocardial injuries through PI3K/Akt signaling pathway, thereby protecting the myocardial cells.

中文翻译：

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红景天苷通过PI3K/Akt通路减轻急性缺氧心肌损伤的机制

 客观的

目的：探讨红景天苷通过PI3K/Akt信号通路的抗炎作用及其对大鼠急性缺氧心肌损伤的保护作用。

 方法

选取24只健康雄性SD大鼠作为实验对象。采用随机数字表法将所有大鼠分为4组，每组6只。分组包括正常对照组、红景天苷组、低压缺氧组、低压缺氧+红景天苷组。红景天苷组大鼠在原动物实验室饲养，每天早晨灌胃红景天苷，剂量为35 mg/kg。正常对照组大鼠给予等剂量生理盐水灌胃。低压缺氧+红景天苷组每天早晨给大鼠灌胃红景天苷，剂量为35 mg/kg，在动物缺氧实验模块中喂养。将海拔升高至4000 m，将大鼠关在模块中24 h。低压缺氧组大鼠在相同环境下灌胃等剂量生理盐水，给药后海拔升高至4000 m。比较各组大鼠的血气分析参数、心脏组织病理学变化、心脏指数以及炎症因子IL-6、TNF-α的含量。

 结果

1.各组大鼠心脏指标比较。低压缺氧组与低压缺氧+红景天苷组比较差异有统计学意义（P < 0.05）。 2.比较各组大鼠血气分析结果。低压缺氧组与低压缺氧+红景天苷组差异有显着性（P < 0.05）。 3.低压缺氧组大鼠心肌细胞排列紊乱、形态不一、水肿、变性、坏死、核固缩、大量炎性细胞浸润等。低压缺氧+红景天苷组心肌细胞上述病理变化得到缓解。 4.与低压缺氧组相比，低压缺氧+红景天苷组大鼠体内IL-6、TNF-α浓度明显降低，差异有统计学意义（P < 0.05）。

 结论

红景天苷对低压缺氧所致大鼠心肌损伤具有修复和保护作用。红景天苷的应用可通过PI3K/Akt信号通路减轻低压缺氧所致心肌损伤大鼠的炎症反应，从而保护心肌细胞。