Table 2.
Summary of studies evaluating the effects of statin use in NASH/NAFLD.
| Type of Statin | Study Design |
Diseases | Dose/Day | Results | Comments | Reference |
|---|---|---|---|---|---|---|
| Atorvastatin | Rat | NAFLD | 30 mg/kg | Atorvastatin up-regulated the expression of PPARα, liver fatty acid β-oxidation, and reduced the liver TG | Atorvastatin treatment effectively improved NAFLD-related hyperlipidemia and inhibited liver steatosis, accompanied by modulating the expression of genes for regulating lipid metabolism | [74] |
| Mice | NAFLD-NASH | 4.5 mg/kg | Atorvastatin prevents cholesterol crystal formation, thereby precluding NLRP3 inflammasome activation to prevent further development of NAFLD | Atorvastatin prevents development of hepatic steatosis, inflammation and fibrosis in mice | [85] | |
| Human | Hypercholesteremia | 10 mg | Atorvastatin reduced LDL-C concentrations and the severity of hepatic steatosis | Atorvastatin effectively and safely reduces elevated hepatic enzyme concentrations in hypercholesterolemic patients | [78] | |
| Fluvastatin | Rat | NASH | 5 mg/kg or 10 mg/kg | Fluvastatin reduced steatosis and fibrosis scores, α-SMA protein expression, mRNA expression of pro-inflammatory and pro-fibrogenic genes in livers | Fluvastatin alleviated steatosis-induced HSCs activation and hepatic fibrogenesis through mitigating inflammation and oxidative stress | [75] |
| Rosuvastatin | Human | NASH | 10 mg | Rosuvastatin resulted in complete resolution of NASH in 19 patients, and lipid values were normalized | Rosuvastatin could ameliorate biopsy-proven NASH and reduce the risk of vascular and liver morbidity and mortality in NASH patients | [79] |
| Simvastatin | Mice | NAFLD | 20 mg/kg | Simvastatin restored antioxidant enzyme activity and decreased lipid peroxidation and ALE-RAGE pathway activation | Simvastatin improved microcirculatory function in NAFLD by downregulating oxidative and ALE-RAGE stress and attenuated steatosis, inflammation and fibrosis. | [86] |
NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; PPAR, peroxisome proliferator-activated receptor; TG, triglycerides; NLRP3, NOD-like receptor family pyrin domain-containing 3; LDL-C, low-density lipoprotein cholesterol; α-SMA, alpha-smooth muscle actin; HSCs, hepatic stellate cells; ALE-RAGE, advanced lipoxidation end product-receptors of advanced glycation end products.