D-柠檬烯(5(一甲基四-[1-甲基乙烯基])环己烷)通过减轻氧化应激、炎症和心脏标志物来减少CCl4诱导的心脏毒性。

IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Rana M AlSaffar, Summya Rashid, Sheikh Bilal Ahmad, Muneeb U Rehman, Ishraq Hussain, Sheikh Parvaiz Ahmad, Majid Ahmad Ganaie
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引用次数: 8

摘要

背景:心血管危机在全球范围内迅速发展。大量研究表明,植物多酚通过对抗氧化系统、信号传导和转录途径的作用,影响心血管事件的主要机制。D-柠檬烯是从柑桔果实中提取的一种单环单萜,具有多种药理活性。方法:本实验旨在测定D-柠檬烯对CCl4所致Wistar大鼠心脏损伤的保护作用。用两种剂量的D-柠檬烯对CCl4诱导的心脏损伤进行治疗。进行血清毒性标志物、心脏毒性生物标志物酶、炎症介质、抗氧化剂库、脂质过氧化、脂质图谱和组织学检查。结果:CCl4中毒导致FFA、TC、TG、PL、LDL、VLDL显著升高,HDL降低,以200mg/kg的剂量给予D-柠檬烯可恢复这些变化。CCl4给药也导致脂质氧化和抗氧化活性降低。同时,D-柠檬烯在200mg/kg体重的剂量下抑制LPO,并使体内抗氧化成分恢复正常。CCl4中毒还导致炎症标志物如IL-6、TNF-α、高敏性皮质酮释放因子(Hs-CRF)以及心脏毒性生物标志物如丙氨酸氨基转移酶(ALT)、乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸酶MB(CKMB)和肌钙蛋白I和肌钙蛋白t活性显著增加。D-柠檬烯使所有这些变化恢复正常。组织学进一步证实了我们获得的结果。结论:D-柠檬烯在200mg/kg体重剂量下可改善心脏损伤。自此,D-柠檬烯通过各种信号通路参与介导CCl4诱导的毒性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

D-limonene (5 (one-methyl-four-[1-methylethenyl]) cyclohexane) diminishes CCl<sub>4</sub>-induced cardiac toxicity by alleviating oxidative stress, inflammatory and cardiac markers.

D-limonene (5 (one-methyl-four-[1-methylethenyl]) cyclohexane) diminishes CCl<sub>4</sub>-induced cardiac toxicity by alleviating oxidative stress, inflammatory and cardiac markers.

D-limonene (5 (one-methyl-four-[1-methylethenyl]) cyclohexane) diminishes CCl<sub>4</sub>-induced cardiac toxicity by alleviating oxidative stress, inflammatory and cardiac markers.

D-limonene (5 (one-methyl-four-[1-methylethenyl]) cyclohexane) diminishes CCl4-induced cardiac toxicity by alleviating oxidative stress, inflammatory and cardiac markers.

Background: The cardiovascular crisis is advancing rapidly throughout the world. A large number of studies have shown that plant polyphenols affect major mechanisms involved in cardiovascular events through their action on the antioxidant system, signaling, and transcription pathways. D-limonene, a monocyclic monoterpene obtained from citrus fruits, is reported to possess many pharmacological activities.Methods: The experiment was designed to determine the protective effect of D-limonene against cardiac injury induced by CCl4 in Wistar rats. Rats were treated with two doses of D-limonene against cardiac injury induced by CCl4. Serum toxicity markers, cardiac toxicity biomarker enzymes, inflammatory mediators, anti-oxidant armory, lipid peroxidation, lipid profile, and histology were done.Results: CCl4 intoxication resulted in a substantial rise in FFA, TC, TG, PL, LDL, VLDL, and a reduction in HDL, restoring these changes with the administration of D-limonene at a dosage of 200 mg/kg. CCl4 administration also resulted in lipid oxidation and decreased antioxidant activity. At the same time, D-limonene at a dosage of 200 mg/kg body weight inhibited LPO and restored in vivo antioxidant components to normal. CCl4 intoxication also resulted in a significant increase in inflammatory markers like IL-6, TNF-α, high sensitivity Corticotropin Releasing Factor (Hs-CRF), and biomarkers of cardiac toxicity like alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase MB (CKMB), and Troponin I & troponin-t activities. D-limonene reversed all these changes to normal. Histology further confirmed our obtained results.Conclusion: These findings indicate that D-limonene can ameliorate cardiac injury at a 200 mg/kg body weight dosage. Henceforth, D-Limonene intervenes in mediating CCl4 induced toxicity by various signaling pathways.

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来源期刊
Redox Report
Redox Report 生物-生化与分子生物学
CiteScore
6.10
自引率
0.00%
发文量
28
审稿时长
>12 weeks
期刊介绍: Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included. While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.
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