MedWire News: Curcumin supplementation could help prevent non-alcoholic steatohepatitis (NASH)-related hepatic fibrosis through suppression of low-density lipoprotein (LDL) oxidation, say researchers.
“NASH is characterized by fat accumulation and inflammation in the liver,” explain Anping Chen and Qiaohua Kang (Saint Louis University, Missouri, USA). It also quite commonly accompanies Type 2 diabetes.
Overall, about one-third of individuals with NASH develop the more serious symptoms of hepatic fibrosis and even cirrhosis.
Curcumin, the yellow pigment from the spice turmeric, has been shown to have anti-inflammatory, anti-oxidative, anti-viral, anti-hypercholesterolemic, anti-infective, and anticarcinogenic effects. It has also been suggested as a promising dietary supplement for liver protection.
Curcumin has previously been shown to inhibit the activation of hepatic stellate cells (HSCs), which are involved in progression of hepatic fibrosis.
In this study, Chen and Kang investigated the role of oxidized (ox)-LDL in HSC activation and the effects of curcumin on this process as well as other underlying mechanisms in cultured rat HSCs.
As reported in the journal Laboratory Investigation, they found that curcumin suppresses expression of the rat version of the human gene for lectin-like oxidized LDL receptor-1 (LOX-1), which results in reduced transport of oxLDL into cells.
The suppression of LOX-1 results from interruption of Wnt signaling and peroxisome proliferator-activated receptor-gamma (PPARg) activation.
“These results support our initial hypothesis and demonstrate that ox-LDL stimulates HSC activation, which is eliminated by curcumin by suppressing lox-1 expression by interrupting Wnt signaling and stimulating PPARg activity,” conclude the authors.
They add: “Our observations provide new insights into the molecular mechanisms of curcumin in inhibiting ox-LDL-induced HSC activation and offer a natural anti-fibrotic candidate for the therapeutic treatment and prevention of Type 2 diabetes and NASH-associated hepatic fibrosis.”
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