Shikimic acid, a phenolic acid reverses isoproterenol-induced myocardial infarction in rat model

Q3 Pharmacology, Toxicology and Pharmaceutics Phytomedicine Plus Pub Date : 2025-03-12 DOI:10.1016/j.phyplu.2025.100788
Mudassir Khattak , Irfan Amir Khan , Nabi Shah , Saud A Abdulsamad , Abdulghani A Naeem , Abdul Jabbar Shah
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Abstract

Background

Myocardial infarction (MI), a leading cause of death in ischemic heart disease, may be mitigated by natural phenolic acids due to their antioxidant properties. This study investigates the cardioprotective role of shikimic acid (SA) against isoproterenol (ISO)-induced myocardial infarction in rats.

Methods

Rats were divided into six groups; all received ISO (85 mg/kg/day, s.c) on days 6 and 7, except the control (normal saline). Groups III-V received SA (10, 30, and 50 mg/kg/day, i.p) for seven days, while group VI was given atenolol (10 mg/kg/day, i.p). In-vitro studies were performed on isolated rat aortic rings and right atrium.

Results

SA pretreatment significantly prevented ISO-induced ECG changes (ST elevation, pathological Q wave), reduced cardiac biomarkers (cTnI, CPK, LDH, AST), improved heart histology, and increased tissue viability. Similarly, SA also showed a significant vasorelaxant effect against phenylephrine-induced precontraction, probably by inhibiting the receptor operated Ca2+ channels without having effect on voltage-dependent Ca2+ channels. SA showed mild negative chronotropic and ionotropic effects, potentially reducing MI-related cardiac workload.

Conclusion

These results indicate that SA preventing MI in rats through improving ECG, cardiac biomarkers and histopathological changes; the effect of SA may be attributed to the decrease in Ca2+movement and cardiac workload.

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莽草酸,一种酚酸逆转异丙肾上腺素诱导的大鼠心肌梗死模型
背景心肌梗塞(MI)是缺血性心脏病的主要死因,天然酚酸具有抗氧化作用,可减轻心肌梗塞。本研究探讨了莽草酸(SA)对异丙肾上腺素(ISO)诱发的大鼠心肌梗死的保护作用。方法将大鼠分为六组,除对照组(生理盐水)外,其余各组均在第 6 天和第 7 天接受 ISO(85 毫克/千克/天,静脉注射)治疗。第三至第五组接受 SA(10、30 和 50 毫克/千克/天,静注)治疗,为期七天;第六组接受阿替洛尔(10 毫克/千克/天,静注)治疗,为期七天。结果 SA 能显著预防 ISO 引起的心电图变化(ST 段抬高、病理性 Q 波),降低心脏生物标志物(cTnI、CPK、LDH、AST),改善心脏组织学,提高组织活力。同样,SA 对苯肾上腺素诱导的预收缩也有明显的血管舒张作用,这可能是通过抑制受体操作的 Ca2+ 通道,而对电压依赖性 Ca2+ 通道没有影响。这些结果表明,SA 可通过改善心电图、心脏生物标志物和组织病理学变化来预防大鼠心肌梗死;SA 的作用可能归因于 Ca2+ 运动和心脏工作量的减少。
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Shikimic acid
来源期刊
Phytomedicine Plus
Phytomedicine Plus Medicine-Complementary and Alternative Medicine
CiteScore
3.70
自引率
0.00%
发文量
178
审稿时长
81 days
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