Rutin exhibits hepatoprotective effects in a mouse model of non-alcoholic fatty liver disease by reducing hepatic lipid levels and mitigating lipid-induced oxidative injuries

Liu, Qing Sheng; Pan, Ran; Ding, Lei; Zhang, Fuli; Hu, Linfeng; Ding, Bin; Zhu, Liang; Xia, Yongliang; Dou, Xiaobing

doi:10.1016/j.intimp.2017.05.026

Cited by 105 publications

(56 citation statements)

References 28 publications

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“…A similar protective response of SKK was earlier observed by us in HepG2 cells treated with carbon tetrachloride [ 19 ]. Plant metabolites comprising of rotenoids, catechin, gallic acid, quercetin, rutin, corilagin, and caffeic acid play a major role in the hepatoprotective role of SKK against a wide range of liver ailments [ 19 , 35 , 36 , 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…Quercetin is a known suppressor of SREBP1c and FAS genes involved in lipogenesis [ 36 ]. Similarly, rutin has shown therapeutic efficacy in lowering triglyceride levels and lipid droplet accumulation in preclinical models [ 37 ]. Caffeic acid is a known enhancer of lipolysis via activation of adipose triglyceride lipase activity [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

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Tri-Herbal Medicine Divya Sarva-Kalp-Kwath (Livogrit) Regulates Fatty Acid-Induced Steatosis in Human HepG2 Cells through Inhibition of Intracellular Triglycerides and Extracellular Glycerol Levels

et al. 2020

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Steatosis is characterized by excessive triglycerides accumulation in liver cells. Recently, application of herbal formulations has gained importance in treating complex diseases. Therefore, this study explores the efficacy of tri-herbal medicine Divya Sarva-Kalp-Kwath (SKK; brand name, Livogrit) in treating free fatty acid (FFA)-induced steatosis in human liver (HepG2) cells and rat primary hepatocytes. Previously, we demonstrated that cytosafe SKK ameliorated CCl4-induced hepatotoxicity. In this study, we evaluated the role of SKK in reducing FFA-induced cell-death, and steatosis in HepG2 through analysis of cell viability, intracellular lipid and triglyceride accumulation, extracellular free glycerol levels, and mRNA expression changes. Plant metabolic components fingerprinting in SKK was performed via High Performance Thin Layer Chromatography (HPTLC). Treatment with SKK significantly reduced the loss of cell viability induced by 2 mM-FFA in a dose-dependent manner. SKK also reduced intracellular lipid, triglyceride accumulation, secreted AST levels, and increased extracellular free glycerol presence in the FFA-exposed cells. SKK normalized the FFA-stimulated overexpression of SREBP1c, FAS, C/EBPα, and CPT1A genes associated with the induction of steatosis. In addition, treatment of rat primary hepatocytes with FFA and SKK concurrently, reduced intracellular lipid accumulation. Thus, SKK showed efficacy in reducing intracellular triglyceride accumulation and increasing extracellular glycerol release, along with downregulation of related key genetic factors for FFA-associated steatosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Tri-Herbal Medicine Divya Sarva-Kalp-Kwath (Livogrit) Regulates Fatty Acid-Induced Steatosis in Human HepG2 Cells through Inhibition of Intracellular Triglycerides and Extracellular Glycerol Levels

et al. 2020

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“…Recently, scutellarin [Zhang et al, 2018b], baicalin [Zhang et al, 2018a], and rutin [Liu et al, 2017] have been used successfully to attenuate the effects of NAFLD. It is speculated that these flavonoids exert lipid-lowering effects by activating several different signaling pathways that are able to reduce the biosynthesis of cholesterol, fatty acids, and TG by the liver (AMPK, PPARγ/PGC-1α-Nrf2, and others).…”

Section: Discussionmentioning

confidence: 99%

Grape Leucoanthocyanidin Protects Liver Tissue in Albino Rabbits with Nonalcoholic Hepatic Steatosis

Franklin

Bispo

Sousa‐Rodrigues

et al. 2018

Cells Tissues Organs

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Nonalcoholic fatty liver disease (NAFLD) is a common ailment. It is usually found in association with diabetes or obesity. There are no approved drugs to treat this condition. The study of flavonoid consumption has increased over the decades due to their antioxidative properties, although the literature is scarce when it comes to their effects in liver tissue. The purpose of this study was to evaluate the role of leucoanthocyanidin in nonalcoholic hepatic steatosis. Thirty male albino rabbits were divided in 3 groups. Group 1 had a regular commercial diet. The second group had a regular diet and 10 mL of egg yolk and 1.5 g of pure cholesterol. The rabbits of the third group were on the same regimen as the second, but were also treated with grape leucoanthocyanidin (50 mg/kg/day) for 100 days. On the last day of the experiment, the animals were euthanized, and the livers excised and fixated in a 10% formalin solution. Afterwards, fragments of each liver were removed and histologically processed and analyzed. The stereological evaluation showed that leucoanthocyanidin reduced NAFLD in comparison with the nontreated group. This was also observed in the histological analysis of the liver tissue, as the treated group had less foci of fatty tissue. Leucoanthocyanidin may therefore be a promising substance to treat NAFLD, although further studies are needed.

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“…An abnormal lipid metabolism, such as an increased uptake of lipids and the upregulation of de novo lipogenesis in the liver, is the initial trigger of NAFLD. Lipid overload promotes reactive oxygen species (ROS) generation and peroxidation itself, which causes the release of pro-inflammatory cytokines and inflammatory cellular infiltration [6,7]. The activation of the nuclear factor-κB (NF-κB) inflammatory pathway regulating downstream target genes plays very important roles in the progression of NAFLD.…”

Section: Introductionmentioning

confidence: 99%

Acupuncture on ST36, CV4 and KI1 Suppresses the Progression of Methionine- and Choline-Deficient Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

et al. 2019

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Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide, and its treatment remain a constant challenge. A number of clinical trials have shown that acupuncture treatment has beneficial effects for patients with NAFLD, but the molecular mechanisms underlying its action are still largely unknown. In this study, we established a mouse model of NAFLD by administering a methionine- and choline-deficient (MCD) diet and selected three acupoints (ST36, CV4, and KI1) or nonacupoints (sham) for needling. We then investigated the effects of acupuncture treatment on the progression of NAFLD and the underlying mechanisms. After two weeks of acupuncture treatment, the liver in the needling-nonapcupoint group (NG) mice appeared pale and yellowish in color, while that in the needling-acupoint group (AG) showed a bright red color. Histologically, fewer lipid droplets and inflammatory foci were observed in the AG liver than in the NG liver. Furthermore, the expression of proinflammatory signaling factors was significantly downregulated in the AG liver. A lipid analysis showed that the levels of triglyceride (TG) and free fatty acid (FFA) were lower in the AG liver than in the NG liver, with an altered expression of lipid metabolism-related factors as well. Moreover, the numbers of 8-hydroxy-2′-deoxyguanosine (8-OHdG)-positive hepatocytes and levels of hepatic thiobarbituric acid reactive substances (TBARS) were significantly lower in AG mice than in NG mice. In line with these results, a higher expressions of antioxidant factors was found in the AG liver than in the NG liver. Our results indicate that acupuncture repressed the progression of NAFLD by inhibiting inflammatory reactions, reducing oxidative stress, and promoting lipid metabolism of hepatocytes, suggesting that this approach might be an important complementary treatment for NAFLD.

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Rutin exhibits hepatoprotective effects in a mouse model of non-alcoholic fatty liver disease by reducing hepatic lipid levels and mitigating lipid-induced oxidative injuries

Cited by 105 publications

References 28 publications

Tri-Herbal Medicine Divya Sarva-Kalp-Kwath (Livogrit) Regulates Fatty Acid-Induced Steatosis in Human HepG2 Cells through Inhibition of Intracellular Triglycerides and Extracellular Glycerol Levels

Tri-Herbal Medicine Divya Sarva-Kalp-Kwath (Livogrit) Regulates Fatty Acid-Induced Steatosis in Human HepG2 Cells through Inhibition of Intracellular Triglycerides and Extracellular Glycerol Levels

Grape Leucoanthocyanidin Protects Liver Tissue in Albino Rabbits with Nonalcoholic Hepatic Steatosis

Acupuncture on ST36, CV4 and KI1 Suppresses the Progression of Methionine- and Choline-Deficient Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

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