翠菊甲醇提取物可减轻肾上腺素诱发的心脏损伤

Sahar A. Abou Halek , Hanan M. Rashwan , Hala M. Ebaid , Heba M.A. Abdelrazek , Heba N. Gad El Hak
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引用次数: 0

摘要

研究目的本研究旨在评估 Cleome droserifolia(MEC)甲醇提取物对肾上腺素诱导的大鼠心脏损伤(MI)的潜在心脏保护特性。对照组(Cont)连续 30 天口服蒸馏水,第 31 天和第 32 天皮下注射生理盐水。MEC 100 组连续 30 天口服 MEC 100 毫克/千克,第 31 天和第 32 天皮下注射生理盐水。MEC 200 组连续 30 天口服 MEC 200 毫克/千克,第 31 天和第 32 天皮下注射生理盐水。肾上腺素组(EP)连续 30 天口服蒸馏水,并在第 31 天和第 32 天皮下注射肾上腺素(2 毫克/千克,静脉注射),分两次服用(每次 1 毫克/千克,静脉注射)。MEC 100+Ep 组连续 30 天口服 MEC 100 毫克/千克,并在第 31 天和第 32 天皮下注射肾上腺素(2 毫克/千克,静脉注射),每次分两次注射(1 毫克/千克,静脉注射)。MEC 200+EP 组接受 MEC 200 毫克/千克,口服,连续 30 天,并在第 31 天和第 32 天皮下注射肾上腺素(2 毫克/千克,静脉注射),每次分为两个剂量(1 毫克/千克,静脉注射)。对心电图(ECG)、生化、氧化应激、炎症介质、组织病理学、免疫组化分析以及磷脂酰肌醇3-激酶(PI3K)和蛋白激酶B(AKT)的表达进行了评估。结果 MEC逆转了肾上腺素引起的心率减慢、QT间期延长和ST位移。MEC预处理可明显降低心肌梗死大鼠的血清天冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)和肌酸激酶-MB(CK-MB)水平。MEC 预处理可提高总抗氧化能力(TAC)、谷胱甘肽(GSH)和总氧化状态(TOS)。此外,它还降低了 MI 大鼠体内的白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、丙二醛(MDA)和肿瘤坏死因子(TNF-α)。此外,据统计,MEC 还降低了心脏组织中核因子-κB(NF-κB)的免疫组化促进作用以及 AKT 和 PI3K 的表达,并改善了组织病理学变化。这种作用是通过改善心功能、抗氧化状态、减轻心电图模式和组织病理变化以及降低 IL-6、IL-1β、TNF-α 和 NF-κB 来实现的,其抗氧化和抗炎潜力可能是部分原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Methanolic extract of Cleome droserifolia mitigates epinephrine-induced cardiac injury

Ethnopharmacological relevance

Cleome droserifolia treatment has potent antioxidant, antimicrobial, and immunomodulatory potentials, which can help recover the general health status.

Aim of the study

This research aims to estimate the potential cardioprotective properties of the methanolic extract of Cleome droserifolia (MEC) against epinephrine-induced cardiac injury (MI) in rats.

Materials and methods

Thirty-six male Wistar rats were separated equally into 6 groups. The control group (Cont) received oral distilled water for 30 uninterrupted days and was administered subcutaneous saline on the 31st and 32nd days. The MEC 100 group received MEC 100 mg/kg, P.O., for 30 uninterrupted days and administered subcutaneous saline on the 31st and 32nd days. The MEC 200 group received MEC 200 mg/kg, P.O. for 30 uninterrupted days and subcutaneous saline was administered on the 31st and 32nd days. The epinephrine group (EP) received distilled water orally for 30 uninterrupted days and administered subcutaneous epinephrine (2 mg/kg, s.c.) divided into two doses (1 mg/kg, s.c) each on the 31st and 32nd days. MEC 100+Ep group received MEC 100 mg/kg, P.O., for 30 uninterrupted days and administered subcutaneous epinephrine (2 mg/kg, s.c.) divided into two doses (1 mg/kg, s.c) each on the 31st and 32nd days. The MEC 200+EP received MEC 200 mg/kg, P.O. for 30 uninterrupted days and administered subcutaneous epinephrine (2 mg/kg, s.c.) divided into two doses (1 mg/kg, s.c) each on the 31st and 32nd days. Electrocardiography (ECG), biochemical, oxidative stress, inflammatory mediators, histopathological, immunohistochemical analysis and the expression of phosphoinositide 3-kinases (PI3K) and protein kinase B (AKT) were assessed.

Results

MEC reversed epinephrine-induced lessening of heart rate, prolonged QT interval and ST displacement. Pretreatment with MEC significantly reduced serum aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) levels in MI rats. The MEC pretreatment promoted total antioxidant capacity (TAC), glutathione (GSH), and total oxidant status (TOS). In addition, it reduced interleukin-1β (IL-1β), interleukin-6 (IL-6), malondialdehyde (MDA), and tumour necrosis factor (TNF-α) in MI rats. Furthermore, MEC statistically reduced immunohistochemical promotion of nuclear factor–κB (NF-κB) and expression of AKT and PI3K in cardiac tissue and perfected histopathological changes.

Conclusion

The MEC, rich in phenolic and flavonoid contents, had a cardioprotective effect on rats suffering from epinephrine-induced MI. Such effect was achieved via improving cardiac function, antioxidant status, attenuating ECG pattern and histological picture, as well as reducing IL-6, IL-1β, TNF-α and NF-κB, which its antioxidant and anti-inflammatory potential may partly arbitrate.

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