A combination of Pueraria lobata and Silybum marianum protects against alcoholic liver disease in mice

Feng, Ruibing; Chen, Jiehua; Liu, Conghui; Xia, Fangbo; Xiao, Zeyu; Zhang, Xuguang; Wan, Jian‐Bo

doi:10.1016/j.phymed.2019.152824

Cited by 33 publications

(25 citation statements)

References 47 publications

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“…The A. absinthium has hepatoprotective effects. The study corroborates with the work of Feng et al (2019) who administered Pueraria lobata and Silybum marianum extracts to mice with the injured liver that occurred after being exposed to excessive alcohol. The extracts showed the most effective protection of alcoholic liver disease.…”

Section: Resultssupporting

confidence: 88%

Evaluation of acute toxicity and sub-acute toxicity of the methanolic extract of Aloe rabaiensis Rendle in BALB/c mice

Mkangara¹,

Mbega²,

Chacha³

2019

J. Med. Plants Res.

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This study was undertaken to evaluate preclinical acute and sub-acute toxicity of Aloe rabaiensis leaf methanolic extract (ARLME) on BALB/c mice following OECD guidelines 423 and 407, respectively. In an acute oral toxicity test, ARLME was administered to the mice by oral gavage at a single dose of 1000, 2000, 3000, 4000 and 5000 mg/Kg body weight. The mice were observed for toxic signs for 14 days. In sub-acute oral toxicity test, ARLME was administered to the mice by oral gavage at 500, 800 and 1000 mg/Kg body weight daily up to 28 th day. At the end of the test, haematological and biochemical analyses of the collected blood sample were carried out as well as gross and microscopic pathology. The control group (F) received a single oral dose of 0.5 mL of 1% DMSO in normal saline. In acute oral toxicity, no treatment-related death or toxic signs at the dosage below 4000 mg/Kg was observed. Nevertheless, at the dosage of 4000 and 5000 mg/Kg, drowsiness and sedation were observed. It was, therefore, revealed that ARLME could be tolerated up to the dose of 3000 mg/Kg body weight and may be classified as category 5. Sub-acute toxicity study at dosage 500 and 800 mg/Kg displayed no adverse changes in the haematological parameter, body weights and histopathological examination. However, at a dosage of 1000 mg/Kg, the serum biochemical aspartate transaminase and alanine transaminase increased, and in histopathological examination of liver and kidney, there was a proliferation of bile duct and leucocytes infiltration respectively. Thus, observations from this study indicate that oral administration of ARLME had no adverse toxic effects in BALB/c mice at the dosage below 1000 mg/Kg, hence supports the use of Aloe rabaiensis in drug formulations.

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Section: Resultssupporting

confidence: 88%

Evaluation of acute toxicity and sub-acute toxicity of the methanolic extract of Aloe rabaiensis Rendle in BALB/c mice

Mkangara¹,

Mbega²,

Chacha³

2019

J. Med. Plants Res.

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“…These data suggest that dietary OFO exacerbates hepatic inflammation upon alcohol challenge. Activation of Kupffer cell via TLR4/NF-κB signaling plays a vital role in hepatic inflammation induced by ethanol exposure 4,30 . Next, we examined the protein expressions of the genes related to TLR4/NF-κB signaling in the liver.…”

Section: Resultsmentioning

confidence: 99%

Oxidation of fish oil exacerbates alcoholic liver disease by enhancing intestinal dysbiosis in mice

Feng

Wang

et al. 2020

Commun Biol

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The role of n-3 polyunsaturated fatty acids (PUFAs) in alcoholic liver disease (ALD) has been controversial. N-3 PUFA oxidation in animal feeding stuffs was rarely concerned, likely contributing to inconsistent outcomes. Here, we report the impacts of oxidized fish oil (OFO) on ALD in C57BL/6 mice. Alcohol exposure increased plasma aminotransferase levels and hepatic inflammation. These deleterious effects were ameliorated by unoxidized FO but exacerbated by OFO. Sequencing analysis showed the accentuated intestinal dysbiosis and the increased proportion of Proteobacteria in OFO-fed mice. Intestinal sterilization by antibiotics completely abolished OFO-aggravated liver injury. Additionally, alcohol exposure leads to the greater increase in plasma endotoxin and decrease in intestinal tight junction protein expressions in OFO-fed mice. Stabilization of intestinal barrier by obeticholic acid markedly blunted OFO-aggravated liver injury in alcohol-fed mice. These results demonstrate that OFO exacerbates alcoholic liver injury through enhancing intestinal dysbiosis, barrier dysfunction, and hepatic inflammation mediated by gut-derived endotoxin.

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“…The methodology for establishing the mice model with alcohol-induced acute liver injury was modified according to previous studies [27, 28]. The mice were randomly divided into six groups ( n = 10/group).…”

Section: Methodsmentioning

confidence: 99%

Hepatoprotective Effects ofMorchella esculentaagainst Alcohol-Induced Acute Liver Injury in the C57BL/6 Mouse Related to Nrf-2 and NF-κB Signaling

Meng

Zhang

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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This study investigated the hepatoprotective effects of Morchella esculenta fruit body (ME) and the underlying mechanisms in mice with alcohol-induced acute liver injury. Systematic analysis revealed that ME contained 21 types of fatty acid, 17 types of amino acid, and 12 types of mineral. Subsequently, a mouse model of acute alcohol-induced liver injury was established by oral administration of alcohol for 14 days. Fourteen-day administration of ME prevented alcohol-induced increases in alanine aminotransferase and aspartate aminotransferase levels and reduced the activity of acetaldehyde dehydrogenase in blood serum and liver tissue. ME appears to regulate lipid metabolism by suppressing triglycerides, total cholesterol, and high-density lipoprotein in the liver. ME inhibited the production of inflammatory factors including chitinase-3-like protein 1 (YKL 40), interleukin-7 (IL-7), plasminogen activator inhibitor type 1 (PAI-1), and retinol-binding protein 4 (RBP4) in blood serum and/or liver tissue. ME treatment relieved the alcohol-induced imbalance in prooxidative and antioxidative signaling via nuclear factor-erythroid 2-related factor 2 (Nrf-2), as indicated by upregulation of superoxide dismutase-1, superoxide dismutase-2, catalase, heme oxygenase-1, and heme oxygenase-2 expression and downregulation of kelch-like ECH-associated protein 1 (Keap-1) in the liver. Moreover, ME reduced the levels of phosphorylated nuclear factor kappa-B kinase α/β, inhibitor of nuclear factor kappa-B α and nuclear factor kappa-B p65 (NF-κB p65) in the liver. The hepatoprotective effects of ME against alcohol-induced acute liver injury were thus confirmed. The mechanism of action may be related to modulation of antioxidative and anti-inflammatory signaling pathways, partially via regulation of Nrf-2 and NF-κB signaling.

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A combination of Pueraria lobata and Silybum marianum protects against alcoholic liver disease in mice

Cited by 33 publications

References 47 publications

Evaluation of acute toxicity and sub-acute toxicity of the methanolic extract of Aloe rabaiensis Rendle in BALB/c mice

Evaluation of acute toxicity and sub-acute toxicity of the methanolic extract of Aloe rabaiensis Rendle in BALB/c mice

Oxidation of fish oil exacerbates alcoholic liver disease by enhancing intestinal dysbiosis in mice

Hepatoprotective Effects ofMorchella esculentaagainst Alcohol-Induced Acute Liver Injury in the C57BL/6 Mouse Related to Nrf-2 and NF-κB Signaling

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