Inhibitory effect of dietary capsaicin on liver fibrosis in mice

Bitencourt, Shanna; Stradiot, Leslie; Verhulst, Stefaan; Thoen, Lien; Mannaerts, Inge; Grunsven, Leo A. van

doi:10.1002/mnfr.201400649

Cited by 17 publications

(13 citation statements)

References 32 publications

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“…Our results showed that CPS administration dose-dependently inhibited serum hepatotoxicity and hepatic lipid peroxidation and increased the weights of body and liver in DMN-treated rats. These results are accordance with those in previously reported studies , and demonstrate the protective effect of CPS in the setting of chronic liver diseases.…”

Section: Discussionsupporting

confidence: 94%

Capsaicin Inhibits Dimethylnitrosamine-Induced Hepatic Fibrosis by Inhibiting the TGF-β1/Smad Pathway via Peroxisome Proliferator-Activated Receptor Gamma Activation

Choi

Jin

Choi³

et al. 2017

J. Agric. Food Chem.

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Capsaicin (CPS) exerts many pharmacological effects, but any possible influence on liver fibrosis remains unclear. Therefore, we evaluated the inhibitory effects of CPS on dimethylnitrosamine (DMN) and TGF-β1-induced liver fibrosis in rats and hepatic stellate cells (HSCs). CPS inhibited DMN-induced hepatotoxicity, NF-κB activation, and collagen accumulation. CPS also suppressed the DMN-induced increases in α-SMA, collagen type I, MMP-2, and TNF-α. In addition, CPS inhibited DMN-induced TGF-β1 expression (from 2.3 ± 0.1 to 1.0 ± 0.1) and Smad2/3 phosphorylation (from 1.5 ± 0.1 to 1.1 ± 0.1 and from 1.6 ± 0.1 to 1.1 ± 0.1, respectively) by activating Smad7 expression (from 0.1 ± 0.0 to 0.9 ± 0.1) via PPAR-γ induction (from 0.2 ± 0.0 to 0.8 ± 0.0) (p < 0.05). Furthermore, in HSCs, CPS inhibited the TGF-β1-induced increases in α-SMA and collagen type I expression, via PPAR-γ activation. These results indicate that CPS can ameliorate hepatic fibrosis by inhibiting the TGF-β1/Smad pathway via PPAR-γ activation.

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Section: Discussionsupporting

confidence: 94%

Capsaicin Inhibits Dimethylnitrosamine-Induced Hepatic Fibrosis by Inhibiting the TGF-β1/Smad Pathway via Peroxisome Proliferator-Activated Receptor Gamma Activation

Choi

Jin

Choi³

et al. 2017

J. Agric. Food Chem.

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“…Bitencourt S et al, at EASL 50 th International Liver Congress, Vienna, stated the inhibitory effects of capsaicin as a dietary supplement on HSC activity in mice with arti icially induced liver ibrosis. Mice fed capsaicin prior to toxin exposure were protected against the development of liver injury and up-regulation of ibrosis activation markers (Bitencourt, 2015).…”

Section: Capsaicinmentioning

confidence: 99%

Alcoholic Hepatitis – A Fatal Disease

Konda

2021

ijrps

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Liver is the vital organ that metabolizes and excretes nutrients. Failure of the liver leads to death in cases. The complication which causes liver failure is excessive alcohol consumption. Liver metabolizes ethanol and it faces the highest degree of injury by uncontrolled drinking. Alcohol use produces a broad spectrum of diseases; hepatosteatosis, Alcoholic hepatitis, fibrosis & cirrhosis. Pathogenesis of Alcohol related Liver Diseases (ALD) is explained by hepatic lipogenesis, deceleration of hepatic lipid breakdown, defective hepatic lipid export, macrophage induced alcoholic hepatitis (AH), Lipopolysaccharide (LPS) transport into the hepatic bloodstream, Malondialdehyde and acetaldehyde (MAA) adducts formation and hepatocyte stellate cell (HSC) induction. Main symptoms of AH include oxidative stress, metabolism interruption, inflammation, restoration process changes and bacterial byproducts misplacement from the gut into hepatic portal blood circulation. Diagnostic studies of ALD are concluded by medical records, clinical and laboratory declarations. Earlier, Glucocorticoids, Pentoxifylline, TNFα were used in the treatment of AH, alone or combined. Novel treatments include Metadoxine, Caspase inhibitors, Microbiome Modification, Microbial Phage Therapy, and liver transplantation. These treatments are prescribed in combination with addiction psychiatrists, social work, and family counselors. Recent studies confirmed that AH could be prevented by consuming capsaicin daily, which ultimately reduces the global burden.

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“…Some reports show that capsaicin alleviates CCl 4 -induced liver fibrosis in rats and mice, via enhancing peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor-erythroid derived 2-related factor 2 (Nrf2)-associated antioxidation, suppressing tumor necrosis factor α (TNF-α) signaling or autophagy of HSCs activation [18][19][20][21][22]. Furthermore, capsaicin also significantly improves bile duct ligation (BDL)-induced mouse liver fibrosis, which may involve the reduction of F4/80 + (a marker of Kupffer cells) expression [19]. Moreover, capsaicin ameliorates dimethylnitrosamine (DMN)-induced rat liver fibrosis through the suppression of the TGF-β1/Smad pathway mediated by PPARγ activation [23].…”

Section: Capsaicinmentioning

confidence: 99%

A review of edible plant-derived natural compounds for the therapy of liver fibrosis

Wang

Niu

et al. 2022

European Journal of Gastroenterology &Amp; Hepatology

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Liver fibrosis has a high incidence worldwide and is the common pathological basis of many chronic liver diseases. Liver fibrosis is caused by the excessive deposition of extracellular matrix and concomitant collagen accumulation in livers and can lead to the development of liver cirrhosis and even liver cancer. A large number of studies have provided evidence that liver fibrosis can be blocked or even reversed by appropriate medical interventions. However, the antifibrosis drugs with ideal clinical efficacy are still insufficient. The edible plant-derived natural compounds have been reported to exert effective antifibrotic effects with few side-effects, representing a kind of promising source for the treatment of liver fibrosis. In this article, we reviewed the current progress of the natural compounds derived from dietary plants in the treatment of liver fibrosis, including phenolic compounds (capsaicin, chlorogenic acid, curcumin, ellagic acid, epigallocatechin-3-gallate, resveratrol, sinapic acid, syringic acid, vanillic acid and vitamin E), flavonoid compounds (genistein, hesperidin, hesperetin, naringenin, naringin and quercetin), sulfur-containing compounds (S-allylcysteine, ergothioneine, lipoic acid and sulforaphane) and other compounds (betaine, caffeine, cucurbitacin B, lycopene, α-mangostin, γ-mangostin, ursolic acid, vitamin C and yangonin). The pharmacological effects and related mechanisms of these compounds in in-vivo and in-vitro models of liver fibrosis are focused.

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Inhibitory effect of dietary capsaicin on liver fibrosis in mice

Abstract: Dietary CPS has potential benefits in the therapy of cholestatic liver fibrosis and in the prophylaxis of hepatotoxic-induced liver injury.

Cited by 17 publications

References 32 publications

Capsaicin Inhibits Dimethylnitrosamine-Induced Hepatic Fibrosis by Inhibiting the TGF-β1/Smad Pathway via Peroxisome Proliferator-Activated Receptor Gamma Activation

Capsaicin Inhibits Dimethylnitrosamine-Induced Hepatic Fibrosis by Inhibiting the TGF-β1/Smad Pathway via Peroxisome Proliferator-Activated Receptor Gamma Activation

Alcoholic Hepatitis – A Fatal Disease

A review of edible plant-derived natural compounds for the therapy of liver fibrosis

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