α-蒎烯对四氯化碳诱发的 Wistar 大鼠心脏损伤的保护作用:抗氧化和炎症反应的调节

Abdelrahim Alqudah, Esam Qnais, Omar Gammoh, Yousra Bseiso, Mohammed Wedyan
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摘要

全球心血管疾病的发病率不断攀升,日益引起人们的关注。大量研究证实,植物多酚(包括α-蒎烯--一种存在于多种植物精油中的单环单萜)对心血管的关键机制有显著影响。这些作用是通过影响抗氧化系统、细胞信号传导途径和基因转录过程来实现的。本研究调查了 α-蒎烯对四氯化碳(CCl4)对 Wistar 大鼠心脏损伤的保护作用。大鼠被分为四组:接受生理盐水的对照组、腹腔注射四氯化碳(1 毫升/千克体重)的疾病对照组以及与四氯化碳同时口服 50 毫克/千克和 100 毫克/千克体重剂量的α-蒎烯的两个治疗组,以评估其剂量依赖性效应。我们进行了全面的评估,包括评估血清和心脏毒性生物标志物、炎症介质、抗氧化防御机制、脂质过氧化水平、脂质概况和组织病理学分析。接触四氯化碳会导致游离脂肪酸(FFA)、总胆固醇(TC)、甘油三酯(TG)、磷脂(PL)、低密度脂蛋白(LDL)和极低密度脂蛋白(VLDL)水平显著升高,而高密度脂蛋白(HDL)水平下降。100 毫克/千克的α-蒎烯能有效抵消这些血脂变化。CCl4 还会导致脂质氧化和抗氧化活性降低,而使用每公斤体重 100 毫克的 α-蒎烯处理后,脂质氧化和抗氧化活性可恢复到正常水平。此外,α-蒎烯还能逆转 CCl4 中毒引起的炎症标志物(白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和高敏 C 反应蛋白(Hs-CRP))和心脏毒性生物标志物(肌酸激酶(CK)、肌酸激酶-心肌带(CK-MB)和肌钙蛋白)的升高。组织病理学研究进一步验证了这些发现。研究得出结论,α-蒎烯的剂量为 100 毫克/千克体重,可有效缓解 CCl4 引起的心脏损伤。数据表明,α-蒎烯通过调节参与 CCl4 引发的心脏毒性的各种信号通路来发挥保护作用。
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Protective effects of α-Pinene against carbon tetrachloride-induced cardiac injury in Wistar rats: modulation of antioxidant and inflammatory responses

The escalating global burden of cardiovascular diseases is a growing concern. Numerous research studies have established that plant-derived polyphenols, including α-pinene—a monocyclic monoterpene found in various plant essential oils—have significant effects on key cardiovascular mechanisms. These effects are mediated through their influence on antioxidant systems, cellular signaling pathways, and gene transcription processes. This study investigated the protective effects of α-pinene against cardiac damage caused by carbon tetrachloride (CCl4) in Wistar rats. Rats were divided into four groups: a control group receiving saline, a disease control group-administered CCl4 (1 mL/kg body weight, intraperitoneally), and two treatment groups receiving α-pinene orally at doses of 50 mg/kg and 100 mg/kg body weight alongside CCl4, to assess its dose-dependent effects. We conducted comprehensive evaluations, including assessments of serum and cardiac toxicity biomarkers, inflammatory mediators, antioxidant defense mechanisms, lipid peroxidation levels, lipid profiles, and histopathological analyses. CCl4 exposure resulted in notable increases in free fatty acids (FFA), total cholesterol (TC), triglycerides (TG), phospholipids (PL), low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL) levels, and a decrease in high-density lipoprotein (HDL) levels. Treatment with α-pinene at 100 mg/kg effectively counteracted these lipid profile changes. CCl4 also caused lipid oxidation and a reduction in antioxidant activities, which were restored to normal levels with α-pinene treatment at 100 mg/kg body weight. Moreover, an upsurge in inflammatory markers (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and high-sensitivity C-reactive protein (Hs-CRP)) and cardiac toxicity biomarkers (creatine kinase (CK), and creatine kinase-myocardial band (CK-MB) and troponin) induced by CCl4 intoxication was reversed by α-pinene. Histopathological studies further validated these findings. The study concludes that α-pinene, administered at a dosage of 100 mg/kg body weight, effectively alleviates cardiac injury induced by CCl4. The data suggest that α-pinene exerts its protective effects through modulation of various signaling pathways involved in CCl4-induced cardiac toxicity.

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