Probiotic and hepatoprotective activity of lactobacillus isolated from Mongolian camel milk products

The improving-intestinal-microbial-balance properties of lactic acid bacteria (LAB) are well known. Thus, LAB could play a vital role in the pathogenesis of liver diseases. In the present study, 107 LAB strains were isolated from Mongolian camel milk products and identified to species, then screened for their probiotic properties. As a result, we identified 71 Lactobacillus bacteria belonging to 9 different species, and 36 Lactococcus bacteria belonging to 8 different species. Among them, six strains of LAB with strong tolerance and adhesion ability were further studied for their protective effect on acute liver injury induced by lipopolysaccharide (LPS)/D-galactosamine (D-GalN). These six strains of LAB were fed to mice for 7 weeks, and on the final day of the experiment, LPS/D-GalN were used to induce acute liver injury. After challenging, the degree of liver pathological changes, secretion of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum and liver, and the expression of tumour necrosis factor (TNF)-α and interleukin (IL)-6 in the liver and intestines were observed and quantified. The results showed that the degree of liver pathological changes in mice fed with the six LAB strains were relieved to varying degrees compared with the LPS/D-GalN-induced model group, and the expressions of AST, ALT, IL-6, and TNF-α factor were also significantly decreased. Moreover, the expression levels of these factors in mice pretreated with Lactobacillus paracasei subsp. paracasei WXD5 were significantly decreased compared with other experimental groups. This suggests the probiotic potential and pharmacological value of L. paracasei subsp. paracasei as a liver injury inhibitor in the intervention of inflammation-based liver disease.

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Hepatoprotective Effect ofShidagonglaoon Acute Liver Injury Induced by Carbon Tetrachloride

The American Journal of Chinese Medicine ◽

10.1142/s0192415x0900751x ◽

2009 ◽

Vol 37 (06) ◽

pp. 1085-1097 ◽

Cited By ~ 9

Author(s):

Jung Chao ◽

Meng-Shiou Lee ◽

Sakae Amagaya ◽

Jiunn-Wang Liao ◽

Jin-Bin Wu ◽

...

Keyword(s):

Carbon Tetrachloride ◽

Liver Injury ◽

Acute Liver Injury ◽

Ethanol Extract ◽

Neutrophil Infiltration ◽

Treated Group ◽

Hepatoprotective Activity ◽

Hepatoprotective Effect ◽

Oxidative Enzymes ◽

Tnf Α

This study investigates the hepatoprotective activity of ethanol extract from Shidagonglao roots (SDGLEtOH). The hepatoprotective effect of SDGLEtOH(20, 100 and 500 mg/kg) was analyzed on carbon tetrachloride ( CCl4)-induced acute liver injury. Rats pretreated orally with SDGLEtOH(100 and 500 mg/kg) and silymarin (200 mg/kg) for 3 consecutive days prior to the administration of a single dose of 50% CCl4(0.10 ml/100 g of bw, ip) significantly prevented the increases in the activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in CCl4-treated rats. Histological analysis also showed that SDGLEtOH(100 and 500 mg/kg) and silymarin reduced the incidence of liver lesions including vacuole formation, neutrophil infiltration and necrosis of hepatocytes induced by CCl4in rats. Moreover, the SDGLEtOH(100 and 500 mg/kg) increased the activities of anti-oxidative enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GRd) and decreased malondialdehyde (MDA) level in liver, as compared to those in the CCl4-treated group. Furthermore, SDGLEtOH(100 and 500 mg/kg) and silymarin attenuated the increased levels of tumor necrosis factor-α (TNF-α) in serum and nitric oxide ( NO ) in liver as compared to the CCl4-treated group. The hepatoprotective mechanisms of SDGLEtOHare likely related to inhibition of TNF-α, MDA and NO productions via increasing the activities of antioxidant enzymes (SOD, GPx and GRd). These experimental results suggest that SDGLEtOHcan attenuate CCl4-induced acute liver injury in rats.

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Protective Effect of Polydeoxyribonucleotide Against CCl4-Induced Acute Liver Injury in Mice

International Neurourology Journal ◽

10.5213/inj.2040430.215 ◽

2020 ◽

Vol 24 (Suppl 2) ◽

pp. 88-95

Author(s):

Seunghwan Lee ◽

Kyu Yeoun Won ◽

Sunhyung Joo

Keyword(s):

Liver Injury ◽

Intraperitoneal Injection ◽

Acute Liver Injury ◽

B Cell Lymphoma ◽

Terminal Deoxynucleotidyl Transferase ◽

Treatment Groups ◽

Accelerate Wound Healing ◽

Tnf Α ◽

Hematoxylin And Eosin ◽

Urogenital Injury

Purpose: Polydeoxyribonucleotide (PDRN) is a substance known to suppress inflammation and accelerate wound healing. In this experiment, the effect of PDRN treatment on carbon tetrachloride (CCl4)-evoked acute liver injury (ALI) was investigated using mice.Methods: We analyzed the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and conducted hematoxylin and eosin staining in accompany with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Western blot analysis was also conducted to assess the expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, adenosine A2A receptor, Bcl-2-associated X protein (Bax), and B-cell lymphoma 2 (Bcl-2). The mice were received intraperitoneal injection of 10-mL/kg CCl4, 4 times, once every 2 days. The mice in the PDRN treatment groups received intraperitoneal injection of 200-μL distilled water comprising each concentration of PDRN for 7 days starting 1 day after first CCl4 injection.Results: ALT and AST concentrations in the serum were reduced and TNF-α, IL-1β, and IL-6 expressions were decreased by PDRN injection in CCl4-evoked ALI mice. PDRN injection suppressed Bax versus Bcl-2 ratio and reduced the percentage of TUNE-positive cells in CCl4-evoked ALI mice. PDRN injection overexpressed adenosine A2A receptor in CCl4-evoked ALI mice.Conclusions: The therapeutic efficacy of PDRN also can be expected for CCl4-evoked acute urogenital injury in addition to ALI. The current research suggests that PDRN may be used for the therapeutic agent of CCl4-evoked ALI.

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Puerarin mitigates acute liver injury in septic rats by regulating proinflammatory factors and oxidative stress levels

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v20i11.11 ◽

2021 ◽

Vol 20 (11) ◽

pp. 2305-2310

Author(s):

Jinan Zheng ◽

Qing Huang ◽

Jingjing Fang

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Acute Liver Injury ◽

Serum Levels ◽

Expression Level ◽

Sepsis Group ◽

Control Group ◽

Sprague Dawley ◽

Tnf Α ◽

Proinflammatory Factors

Purpose: To determine the protective effect of puerarin against acute liver injury in septic rats, and the mechanism involved.Methods: Eighty-seven Sprague-Dawley (SD) rats were assigned to control, sepsis and puerarin groups (each having 29 rats). Serum levels of NF-kB, TNF-α, IL-1 β, IL-6, ALT and AST were assayed. Liver lesions and levels of NO, SOD, iNOS and malondialdehyde (MDA) were measured using standard procedures.Results: Compared with the control group, the levels of NF-kB, TNF-α, IL-1β, IL-6, AST, ALT, NO, MDA and iNOS significantly increased in the sepsis group, while SOD level decreased significantly. In contrast, there were marked decreases in NF-kB, TNF-α, IL-1β, AST, ALT, NO, MDA and iNOS in puerarin group, relative to the sepsis group, while SOD expression level was significantly increased (p <0.05). The level of p-p38 in liver of septic rats was up-regulated, relative to control rats, while Nrf2 significantly decreased (p < 0.05). The expression level of p-p38 in the puerarin group was significantly decreased, relative to the sepsis group, while the expression level of Nrf2 significantly increased (p < 0.05).Conclusion: Puerarin mitigates acute liver injury in septic rats by inhibiting NF-kB and p38 signaling pathway, down-regulating proinflammatory factors, and suppressing oxidative stress. Thus, puerarin may be developed for use in the treatment liver injury.

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S100A6 Promotes Inflammation and Infiltration of Mononuclear/Macrophages via the p-P38 and p-JNK Pathways in Acute Liver Injury

10.21203/rs.3.rs-1161048/v1 ◽

2021 ◽

Author(s):

He Tong ◽

Li Wang ◽

Kefan Zhang ◽

Jing Shi ◽

yongshuai Wu ◽

...

Keyword(s):

Liver Injury ◽

Inflammatory Response ◽

Inflammatory Responses ◽

Acute Liver Injury ◽

S100 Protein ◽

Inflammatory Cells ◽

Liver Cells ◽

Danger Signal ◽

Tnf Α

Abstract BackgroundThe phagocytic S100 protein, which mediates inflammatory responses and recruits inflammatory cells to sites of tissue damage, has long been known to be expressed in cells of myeloid origin. S100A6 belongs to the A group of the S100 protein family of Ca2+-binding proteins. Currently, the mechanism by which S100A6 mediates the inflammatory response and recruits inflammatory cells to the tissue injury site is unknown.MethodsA mouse model of carbon tetrachloride (CCl4)-induced acute liver injury (ALI) was established, and the transcriptomes of postinjury 2d and 5d liver tissues were sequenced. Enzyme-linked immunosorbent assay was used to determine the expression of inflammatory factors (TNF-α, IL-1β, IL-6, and IL-8) in the supernatant of the liver. Immunohistochemical analysis confirmed the expression of S100A6 in the liver cells. In vitro experiments proved the pro-inflammatory function of S100A6, and western blotting (WB) showed that the pathways were activated. The transwell experiment showed the infiltration of mononuclear/macrophages.ResultsWe found that S100A6 is highly expressed in liver cells during the most severe period of ALI, suggesting that it acts as an endogenous danger signal and has a pro-inflammatory function. In vitro, the mouse S100A6 recombinant protein was used to stimulate liver Kupffer cells to promote the secretion of TNF-α, IL-1β, IL-6, and IL-8. Further mechanistic experiments revealed that S100A6 acts as an endogenous danger signal to activate p-P38 and p-JNK downstream of the TLR4 and P65 pathways. Similarly, transcriptome data showed that S100A6 can activate the inflammatory response in Kuffer cells. WB revealed that S100A6 had no significant effect on cell apoptosis. To continue to explore the mechanism of monocyte/macrophage infiltration, we found that TNF-α stimulates liver cells as the main source of CCL2. TNF-α can initiate the p-P38 and p-JNK pathways of liver cells to produce CCL2, thereby recruiting the infiltration of mononuclear/macrophages. ConclusionsTaken together, S100A6 is an endogenous danger signal that mediates inflammatory responses and recruits inflammatory cells to sites of tissue damage.

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Target prediction of anti-chronic liver injury of Kangxian pill based on network pharmacology

10.21203/rs.3.rs-547171/v1 ◽

2021 ◽

Author(s):

Min Cao ◽

Yiyang Wang ◽

Haizhao Liu ◽

Xueqian Dong ◽

Mengxue Dong ◽

...

Keyword(s):

Liver Injury ◽

Protein Expression ◽

Molecular Mechanisms ◽

Target Prediction ◽

Vital Role ◽

Chronic Liver ◽

Network Pharmacology ◽

Chronic Liver Injury ◽

Tnf Α

Abstract BackgroundThe present study aimed to validate the protect effect of Kangxian pill (KXP) on chronic hepatic injury (CHI) and investigate its potential mechanism by network pharmacology-based prediction and experimental verification in vivo . MethodsThe effect of KXP in the treatment of carbon tetrachloride (CCL 4 )-induced CHI is investigated by calculating liver index, measuring AST and ALT levels and performing HE staining. Targets of active ingredients of KXP were predicted in TCSMP and targets of chronic liver injury were searched in DisGeNET, OMIM and GeneCards databases. We obtain some pivotal targets of KXP for the treatment of CHI by intersecting the targets of KXP and CHI. Subsequently, we performed gene ontology (GO) functional and pathways enrichment analyses, as well as conducted networks based on potential targets to determine the core targets and representative pathways.We further validated expressions of IL-6, IL-1β, TNF-α, Bax, Bcl2, PI3K, Akt, and pAkt according to the potential molecular mechanisms analyzed based on network pharmacology analysis.ResultsThe results showed that the levels of AST and ALT in serum decreased after treatment with KXP. HE staining also revealed that KXP could improve hepatocyte abnormality in vivo . A total of 81 potential targets of KXP in the treatment of CHI were identified through network pharmacology analysis. After integrating potential targets, function enrichment, representative pathways and networks, we identified PI3K, AKT1,BCL2, TNF-α, IL-1β, and IL-6 as potential targets, which may play a vital role in the KXP treatment. The experimental results also showed that KXP could down-regulate the mRNA and protein expression of IL-1β, IL-6, TNF-α and Bax, and up-regulate the PI3K and p-Akt protein expression i n vivo .ConclusionsOur results suggest that KXP could alleviate CHI through regulating inflammation and apoptosis and provide deep insight into the hepato-protective mechanisms.

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Hepatoprotective activity of petroleum ether, diethyl ether, and methanol extract of Scoparia dulcis L. against CCl4-induced acute liver injury in mice

Indian Journal of Pharmacology ◽

10.4103/0253-7613.55206 ◽

2009 ◽

Vol 41 (3) ◽

pp. 110 ◽

Cited By ~ 4

Author(s):

MJ Nanjan ◽

Rema Razdan ◽

TK Praveen ◽

S Dharmaraj ◽

Jitendra Bajaj ◽

...

Keyword(s):

Liver Injury ◽

Petroleum Ether ◽

Diethyl Ether ◽

Methanol Extract ◽

Acute Liver Injury ◽

Hepatoprotective Activity ◽

Scoparia Dulcis

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Hepatoprotective Effects of Chai-Hu-Ching-Kan-Tang on Acetaminophen-Induced Acute Liver Injury in Rats

The American Journal of Chinese Medicine ◽

10.1142/s0192415x07004631 ◽

2007 ◽

Vol 35 (01) ◽

pp. 69-79 ◽

Cited By ~ 5

Author(s):

Tzu-Hsiang Lin ◽

Lean-Teik Ng ◽

Feng-Lin Yen ◽

Chun-Ching Lin

Keyword(s):

Liver Injury ◽

Liver Diseases ◽

Acute Liver Injury ◽

Lipid Peroxides ◽

Hepatoprotective Activity ◽

Glutamic Pyruvic Transaminase ◽

Glutamic Oxaloacetic Transaminase ◽

Serum Glutamic Oxaloacetic Transaminase ◽

Hepatoprotective Agent ◽

Hepatoprotective Effects

Chai-Hu-Ching-Kan-Tang (CHCKT) is one of the traditional Chinese medicine prescriptions commonly used to treat liver diseases. In this study, we evaluated the hepatoprotective effects of aqueous CHCKT extract at various concentrations (125, 250 and 500 mg/kg body weight) on acetaminophen (APAP)-induced acute liver injury in rats. Results showed that CHCKT treatments significantly decreased the level of serum glutamic oxaloacetic transaminase (sGOT) and glutamic pyruvic transaminase (sGPT) in APAP-treated groups. CHCKT also significantly decreased the level of lipid peroxides and increased the activity of antioxidant enzymes (i.e. SOD and GPx). Histopathological observation further confirmed the hepatoprotective activity of CHCKT as indicated by the amelioration in the central necrosis and fatty changes of the liver after APAP induction. Interestingly, the hepatoprotective activity of CHCKT at concentrations 125~500 mg/kg appeared to be as good as 12.5 mg/kg silymarin (a commercial hepatoprotective agent). Taken together, these results suggest that aqueous extract of CHCKT possesses potent hepatoprotective effects agianst APAP-induced liver injury in rats.

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Protective effect of Trillium tschonoskii saponin on CCl4-induced acute liver injury of rats through apoptosis inhibition

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2016-0228 ◽

2016 ◽

Vol 94 (12) ◽

pp. 1291-1297 ◽

Cited By ~ 18

Author(s):

Hao Wu ◽

Yong Qiu ◽

Ziyang Shu ◽

Xu Zhang ◽

Renpeng Li ◽

...

Keyword(s):

Liver Injury ◽

Caspase 3 ◽

Acute Liver Injury ◽

Protective Role ◽

High Dose ◽

Dependent Manner ◽

Hepatocyte Apoptosis ◽

Liver Index ◽

Tnf Α ◽

Trillium Tschonoskii

To explore hepatoprotective role and underlying mechanisms of Trillium tschonoskii Maxim (TTM), 36 rats were randomly divided into control, CCl4-induced liver injury model, and biphenyl dimethyl dicarboxylate (DDB) and low-, moderate-, and high-dose TTM treatment groups. After CCl4-induced model establishment, the rats from DDB and TTM groups were administrated with DDB at 0.2 g/kg per day and TTM at 0.1, 0.5, and 1.0 g/kg per day, while the rats from control and model groups were administrated with saline. After 5 days of treatments, all rats were sacrificed for determining serum ALT and AST levels and liver index, examining histopathological changes in liver through HE and TUNEL staining, and evaluating TNF-α and IL-6 mRNA expression by real-time PCR, and caspase-3, Bcl-2, and Bax expression by Western blot. Results indicated that CCl4 could induce acute liver injury and abnormal liver function in rats with obvious hepatomegaly, increased liver index, high ALT and AST levels, up-regulated TNF-α and IL-6, and overexpressed Bax and caspase-3. However, DDB and TTM could execute protective role in CCl4-induced liver injury in rats through reducing ALT and AST levels, rescuing hepatomegaly, down-regulating inflammatory factors and inhibiting hepatocyte apoptosis in a dose-dependent manner. Therefore, TTM has obvious protective role in CCl4-induced liver injury of rats through inhibiting hepatocyte apoptosis.

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Hepatoprotective Effects of Different Extracts From Triphala Against CCl4-Induced Acute Liver Injury in Mice

Frontiers in Pharmacology ◽

10.3389/fphar.2021.664607 ◽

2021 ◽

Vol 12 ◽

Author(s):

Xichuan Wei ◽

Chuanhong Luo ◽

Yanan He ◽

Haozhou Huang ◽

Fei Ran ◽

...

Keyword(s):

Liver Injury ◽

Mouse Model ◽

Protein Expression ◽

Acute Liver Injury ◽

Quinone Oxidoreductase ◽

Tnf Α ◽

Gene And Protein Expression ◽

Wide Range ◽

Hepatoprotective Effects ◽

The Impact

Background:Triphala is a traditional polyherbal formula used in Indian Ayurvedic and Chinese Tibetan medicine. A wide range of biological activities have been attributed to Triphala, but the impact of various extraction methods on efficacy has not been determined.Purpose: The study aimed to evaluate Triphala extracts obtained by various methods for their hepatoprotective effects and molecular mechanisms in a mouse model of carbon tetrachloride (CCl4)-induced liver injury.Methods: HPLC fingerprinting was used to characterize the chemical characteristics of Triphala extracts obtained by (a) 0.5 h ultrasonication, (b) 2 h reflux, and (c) 4 h reflux. Hepatoprotective efficacy was evaluated in a mouse model of CCl4-induced liver damage. Serum levels of alanine transaminase (ALT) and aspartate aminotransferase (AST) were measured, as well as the liver antioxidant and inflammatory markers malondialdehyde superoxide dismutase glutathione peroxidase (GSH-Px), TNF-α, and IL-6. Gene and protein expression of Nrf-2 signaling components Nrf-2, heme oxygenase (HO-1), and NADPH Quinone oxidoreductase (NQO-1) in liver tissue were evaluated by real-time PCR and western blotting.Results: Chemical analysis showed a clear difference in content between extracts produced by ultrasonic and reflux methods. The pharmacological analysis showed that all three Triphala extracts reduced ALT, AST, MDA, TNF-α, and IL-6 levels and increased SOD and GSH-Px. Triphala extracts also induced transcript and protein expression of Nrf-2, HO-1, and NQO-1.Conclusion: Triphala extract prevents CCl4-induced acute liver injury. The ultrasonic extract of Triphala was most effective, suggesting that hepatoprotection may be related to the larger tannins via activation of Nrf-2 signaling.

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