姜黄素对心脏脂肪毒性的有益影响

IF 2.8 4区 医学 Q2 PHARMACOLOGY & PHARMACY Journal of Pharmacy and Pharmacology Pub Date : 2024-08-24 DOI:10.1093/jpp/rgae102
Sajad Abolfazli, Alexandra E Butler, Prashant Kesharwani, Amirhossein Sahebkar
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引用次数: 0

摘要

脂肪毒性是指长期的脂质代谢失衡,导致脂肪异位分布于肝脏、心脏和肾脏等外周器官。脂质在心肌细胞中过度积聚的有害后果会导致心脏脂肪毒性,从而改变心脏的结构和功能。肥胖和糖尿病与脂毒性心肌病有关。这些异常可能是由于有害的新陈代谢转变造成的,这种转变会积累有毒的脂质,并将葡萄糖氧化转变为较少的脂肪酸氧化。研究发现,脂肪酸、脂肪酰辅酶 A、二酰甘油和神经酰胺与细胞中的脂毒性压力有关。这种应激可由细胞凋亡、胰岛素信号受损、内质网应激、蛋白激酶 C 激活、p38 Ras-丝裂原活化蛋白激酶(MAPK)激活或过氧化物酶体增殖激活受体(PPARs)家族成员的改变引起。姜黄素是一种疏水性多酚衍生物,具有多种药理特性。多年来,姜黄素一直被用作抗炎、抗氧化、抗癌、保肝、保心、抗糖尿病和抗肥胖药物。姜黄素通过抑制细胞凋亡和减少细胞凋亡相关蛋白的表达、减少炎症细胞因子的表达、激活自噬信号通路以及抑制内质网应激标志蛋白的表达,来降低心脏脂肪毒性。
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The beneficial impact of curcumin on cardiac lipotoxicity.

Lipotoxicity is defined as a prolonged metabolic imbalance of lipids that results in ectopic fat distribution in peripheral organs such as the liver, heart, and kidney. The harmful consequences of excessive lipid accumulation in cardiomyocytes cause cardiac lipotoxicity, which alters the structure and function of the heart. Obesity and diabetes are linked to lipotoxic cardiomyopathy. These anomalies might be caused by a harmful metabolic shift that accumulates toxic lipids and shifts glucose oxidation to less fatty acid oxidation. Research has linked fatty acids, fatty acyl coenzyme A, diacylglycerol, and ceramide to lipotoxic stress in cells. This stress can be brought on by apoptosis, impaired insulin signaling, endoplasmic reticulum stress, protein kinase C activation, p38 Ras-mitogen-activated protein kinase (MAPK) activation, or modification of peroxisome proliferator-activated receptors (PPARs) family members. Curcuma longa is used to extract curcumin, a hydrophobic polyphenol derivative with a variety of pharmacological characteristics. Throughout the years, curcumin has been utilized as an anti-inflammatory, antioxidant, anticancer, hepatoprotective, cardioprotective, anti-diabetic, and anti-obesity drug. Curcumin reduces cardiac lipotoxicity by inhibiting apoptosis and decreasing the expression of apoptosis-related proteins, reducing the expression of inflammatory cytokines, activating the autophagy signaling pathway, and inhibiting the expression of endoplasmic reticulum stress marker proteins.

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来源期刊
CiteScore
6.60
自引率
0.00%
发文量
91
审稿时长
3 months
期刊介绍: JPP keeps pace with new research on how drug action may be optimized by new technologies, and attention is given to understanding and improving drug interactions in the body. At the same time, the journal maintains its established and well-respected core strengths in areas such as pharmaceutics and drug delivery, experimental and clinical pharmacology, biopharmaceutics and drug disposition, and drugs from natural sources. JPP publishes at least one special issue on a topical theme each year.
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