Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway.
Kaifeng LiMengen ZhaiLiqing JiangFan SongBin ZhangJie LiHua LiBuying LiLin XiaLu XuYu CaoMengshan HeHanzhao ZhuLiyun ZhangHongliang LiangZhenxiao JinWeixun DuanSi-Wang WangPublished in: Oxidative medicine and cellular longevity (2019)
Hyperglycemia-induced oxidative stress and fibrosis play a crucial role in the development of diabetic cardiomyopathy (DCM). Tetrahydrocurcumin (THC), a major bioactive metabolite of natural antioxidant curcumin, is reported to exert even more effective antioxidative and superior antifibrotic properties as well as anti-inflammatory and antidiabetic abilities. This study was designed to investigate the potential protective effects of THC on experimental DCM and its underlying mechanisms, pointing to the role of high glucose-induced oxidative stress and interrelated fibrosis. In STZ-induced diabetic mice, oral administration of THC (120 mg/kg/d) for 12 weeks significantly improved the cardiac function and ameliorated myocardial fibrosis and cardiac hypertrophy, accompanied by reduced reactive oxygen species (ROS) generation. Mechanically, THC administration remarkably increased the expression of the SIRT1 signaling pathway both in vitro and in vivo, further evidenced by decreased downstream molecule Ac-SOD2 and enhanced deacetylated production SOD2, which finally strengthened antioxidative stress capacity proven by repaired activities of SOD and GSH-Px and reduced MDA production. Additionally, THC treatment accomplished its antifibrotic effect by depressing the ROS-induced TGFβ1/Smad3 signaling pathway followed by reduced expression of cardiac fibrotic markers α-SMA, collagen I, and collagen III. Collectively, these finds demonstrated the therapeutic potential of THC treatment to alleviate DCM mainly by attenuating hyperglycemia-induced oxidative stress and fibrosis via activating the SIRT1 pathway.
Keyphrases
- high glucose
- endothelial cells
- signaling pathway
- anti inflammatory
- reactive oxygen species
- diabetic rats
- oxidative stress
- hydrogen peroxide
- poor prognosis
- wound healing
- epithelial mesenchymal transition
- type diabetes
- pi k akt
- heart failure
- ischemia reperfusion injury
- left ventricular
- cell death
- liver fibrosis
- amyotrophic lateral sclerosis
- transforming growth factor
- induced apoptosis
- combination therapy
- binding protein
- human health
- risk assessment
- cell cycle arrest
- atrial fibrillation
- drug induced
- preterm birth
- pulmonary fibrosis
- fluorescent probe