Protective effect of Solanum Nigrum Linn green fruit ethanolic extract on alcoholic liver injury in mice

Alcoholic liver injury is a liver disease caused by excessive alcohol consumption,which can lead to chronic liver disease death.Solanum Nigrum Linn taste bitter,cold,has the effect of clearing heat and detoxification,promoting blood and detumescence.Solanum Nigrum Linn fruit contains a variety of antioxidant enzymes,can remove the body produced by aerobic metabolism harmful substances.In this paper,a model of alcohol-induced liver injury in C57BL/6 mice was established to evaluate the protective effect of Solanum Nigrum Linn green fruit(SNGF)ethanolic extract on alcohol-induced liver injury.H&E staining and oil red O(ORO)staining showed that hepatic lobules were clearly demarcated,vacuoles were significantly reduced and lipid droplets were reduced in SNGF ethanolic extract treatment group.Serum levels of TC,TG,LDH,TBA,AKP,ALT and AST were decreased in the SNGF ethanolic extract treatment group,and SNGF ethanolic extract could clear reactive oxygen species(ROS)in time.MDA content was signifi cantly decreased after SNGF ethanolic extract treatment,while superoxide dismutase(SOD)and GSH-Px contents were increased after SNGF ethanolic extract treatment.These results suggest that SNGF ethanolic extract has a protective effect on alcohol-induced liver injury.

Alcoholic liver injury:Influence of gender and hormones

This article discusses several subjects pertinent to a consideration of the role of gender and hormones in alcoholic liver injury (ALI). Beginning with an overview of factors involved in the pathogenesis of ALI, we review changes in sex hormone metabolism resulting from alcohol ingestion, summarize research that points to estrogen as a cofactor in ALI, consider evidence that gut injury is linked to liver injury in the setting of alcohol, and briefly review the limited evidence regarding sex hormones and gut barrier function. In both women and female animals, most studies reveal a propensity toward greater alcohol-induced liver injury due to female gender, although exact hormonal influences are not yet understood. Thus, women and their physicians should be alert to the dangers of excess alcohol consumption and the increased potential for liver injury in females.

Study on the Protective Effect and Mechanism of Tibetan Medicine Ershiwuwei Songshi Pill on Acute Alcoholic Liver Injury in Rats

[Objectives]To investigate the protective effect and mechanism of Ershiwuwei Songshi Pill on acute alcoholic liver injury in rats.[Methods]Sixty male SD rats were randomly divided into normal control group,model group,polyene phosphatidylcholine(82.08 mg/kg)positive control group and Ershiwuwei Songshi Pill high(180 mg/kg),medium(90 mg/kg)and low(45 mg/kg)dose groups.The rats in each group were given corresponding drugs by intragastric administration for 3 d and fed normally.From the 4th d,all groups except the normal control group were fed with 15 mL/kg liquor(56%vol)for 7 d after 2 h of administration.After the last modeling,the levels of AST,ALT,TC,TG,SOD,GSH in serum and IL-1β,IL-6,TNF-αin liver tissue were measured.The protein expressions of Bax,Bcl-2 and Caspase3 were determined by Western blotting.HE staining was used to observe the pathological changes of liver tissue under light microscope.[Results]Compared with the model group,the body weight and the levels of SOD and GSH in the treatment group were significantly higher than those in the model group;liver index,serum ALT,AST,TC,TG,IL-1β,IL-6 and TNF-αlevels decreased significantly(P<0.01 or P<0.05);HE staining showed that there was a small amount of collagen proliferation and lymphocyte infiltration in connective tissue around the hepatic portal area in the model group,multiple inflammatory foci could be seen in the lobules,and round fat vacuoles could be seen in the cytoplasm;in each administration group,the pathological condition of the liver was mild.[Conclusions]Ershiwuwei Songshi Pill had a certain protective effect on acute alcoholic liver injury in rats,and its mechanism might be related to reducing enzyme,promoting lipid metabolism and anti-inflammation.

Lignans from Seeds of Herpetospermum caudigerum Wall.Protect Against Alcoholic Liver Injury via TGF-β/Smads Pathway in Rats

[Objectives]This study aimed to investigate the effects of lignans from seeds of Herpetospermum caudigerum Wall.(SHC)on expression of TGF-β/Smads in liver tissue of hepatic alcohol-injuried rats,and to explore its protective mechanism.[Methods]A total of 60 SD rats were randomly divided into six groups.The rats in all the groups except those in the normal group were given with white spirit by gavage for 8 weeks to establish alcoholic liver injury models.After rat models were established successfully,they were administered intragastrically with 400,200 and 100 mg/kg of lignans,respectively.The rats in the normal group were administered intragastrically with 50 mg/kg of silymarin.The administration lasted for 8 weeks,once a day.The changes in the general state,liver tissue pathology and collagen deposition of the rats were observed.The expression of TGF-β,TGF-β1 receptor 1(TβR-I),TGF-β1 receptor 2(TβR-II),Smad2/p-Smad2 and Smad3/p-Smad3 in the hepatic tissue was detected.[Results]The expression levels of TGF-β1,Smad2,p-Smad2,and p-Smad3 significantly declined,and the expression levels of TβR-I,TβR-II and Smad3 did not change significantly in the liver tissue of rats in the lignans groups and the expression levels of TGF-β,Smad2,and p-Smad3 significantly declined.Meanwhile,the expression levels of TβR-I,TβR-II,p-Smad2 and Smad3 did not change significantly in the silymarin group.[Conclusions]The lignans from SHC have significant intervention effects on alcoholic livery injury.The mechanism may be related to the inhibition of hepatic stellate cell(HSC)activation,TGF-βsecretion and p-Smad2,p-Smad3 expression in the signaling pathway.

Protective effect of gingerol dropping pills against alcoholic liver injury in mice

OBJECTIVE To prepare gingerol dropping pills and to investigate its protective effect on alcoholic liver injury. METHODS The prescription was selected by orthogonal design method and the effect of the option and ratio of ground substance,the temperature of drug. The hardness,circular degree,the tail formation and the dissolution time were studied. Totally 40 KM mice were randomly divided into control group,model group,gingerol dropping pill group(400 mg·kg^(-1)·d^(-1)) and positive control group(bifendate,150 mg·kg^(-1)·d^(-1)) of 10 mice each. The mice from the model and two drug groups were administrated with liqueur[0.15 mL/(10 g·d)]daily by gavage for 3 weeks,Two hours later,drug group mice were treated corresponding gingerol dropping pill and bifendate. Meanwhile,the control group were gavaged same amount of normal saline. Finally,when the model of acute alcoholic liver injury was established on the 22 stday,Biochemical indicators of ocular blood in mice were observed.We also observed the change of liver morphology. RESULTS Under optimum conditions,we can obtain dropping pills having circular shape,touching with hardness and short dissolution time. Compared with the control group,the levels of alanine transaminase(ALT),glutamic-oxaloacetic transaminase(AST) and malondialdehyde(MDA) in model group were obviously increased(P<0.01),While the activity of Superoxide dismutase(SOD) were decreased. In addition,In model group,mice liver disorders,hepatic lobule fusion,accompanying a large number of patchy sample liver cell vacuoles,various sizes of fat vacuoles appeared in cytoplasm and inflammatory cell infiltration were visible around the central vein. On the contrary,compared with the model group,drug groups attenuated or even reversed hepatic pathological changes. Form gingerol dropping pill group,an increase in hepatic SOD activity and serum ALT and AST activities were found and a significant decrease in hepatic MDA content were also observed(P<0.01). CONCLUSION The prescription of gingerol dropping pills was reasonable,and the preparation process was simple. Gingerol dropping pills can protect liver from alcoholic liver injury to some extend,and the mechanism may be related to its antioxidant effect.

Ameliorative effects of monascin from red mold rice on alcoholic liver injury and intestinal microbiota dysbiosis in mice

Monascus-fermented red mold rice(RMR)has excellent physiological efficacy on lipid metabolism and liver function.This study investigated the ameliorative effects of monascin(MS)from RMR on alcoholic liver injury(ALI)in mice,and further illustrated its mechanism of action.Results indicated that dietary MS intervention obviously ameliorated lipid metabolism and liver function in mice with over-drinking.In addition,MS intervention alleviated alcohol-induced oxidative stress in the liver by reducing the hepatic activities of lactate dehydrogenase(LDH)and hepatic levels of malondialdehyde(MDA),increasing the hepatic activities of catalase(CAT),superoxide dismutase(SOD),alcohol dehydrogenase(ADH)and hepatic levels of glutathione(GSH).16S rRNA amplicon sequencing showed that excessive drinking had a significant effect on the composition of the gut microbiota in mice.MS intervention was beneficial to ameliorate intestinal microbiota dysbiosis by elevating the proportion of Lactobacillus,Lachnospiraceae_UCG-006,Coriobacteriales,etc.,but decreasing the proportion of Staphylococcus,Muribaculaceae,Desulfovibrionaceae,etc.Additionally,correlation analysis indicated that the key intestinal bacterial taxa intervened by MS were closely related to some biochemical indicators of lipid metabolism,liver function and oxidative stress.Moreover,liver metabolomics analysis revealed that dietary MS supplementation significantly regulated the levels of liver metabolites involved in taurine and hypotaurine metabolism,riboflavin metabolism,and purine metabolism,etc.Furthermore,MS intervention regulated gene transcription and protein expression associated with lipid metabolism and oxidative stress in the liver.In short,these findings suggest that MS mitigates alcohol-induced hepatic oxidative damage through modulating the intestinal microbiome and liver metabolic pathway,and thus can be served as a functional component to prevent alcoholic liver disease.

Madelung’s disease with alcoholic liver disease and acute kidney injury: A case report

BACKGROUND Madelung’s disease(MD)is a rare disorder of lipid metabolism,characterized by the growth of unencapsulated masses of adipose tissue symmetrically deposited around the neck,shoulders,or other sites around the body.Its pathological mechanism is not yet known.One of the most common comorbidities in MD patients is liver disease,especially chronic alcoholic liver disease(CALD);however,no reports exist of acute kidney injury(AKI)with MD.CASE SUMMARY We report a 60-year-old man who presented with complaint of edema in the lower limbs that had persisted for 3 d.Physical examination showed subcutaneous masses around the neck,and history-taking revealed the masses to have been present for 2 years and long-term heavy drinking.Considering the clinical symptoms,along with various laboratory test results and imaging characteristics,a diagnosis was made of MD with acute exacerbation of CALD and AKI.The patient was treated with liver function protection and traditional Chinese medicine,without surgical intervention.He was advised to quit drinking.After 10 d,the edema had subsided,renal function indicators returned to normal,liver function significantly improved,and size of subcutaneous masses remained stable.CONCLUSION In MD,concomitant liver or kidney complications are possible and monitoring of liver and kidney functions can be beneficial.

Study on Protection Mechanism of Viscum coloratum (Kom.) Nakai f. lutescens kitag Fruit Polysaccharides on Mice with Acute Alcoholic Liver Injury

This study was conducted to investigate the protective mechanism of V. coloratum fruit polysaccharides（ VCFP） on mice with acute alcoholic liver injury. Acute liver injury model was built by one-time alcohol gavage. The mice were randomly divided into VCFP-treated groups（ low-,medium-,and highdose）,alcohol model group and normal control group at the same time. VCFP-treated groups were administrated polysaccharide intragastrically continuously for4 weeks; and the alcohol model group and normal control group were administrated intragastrically the same amount of normal saline. The general situation and liver tissue morphological structure changes were observed. The results showed that the levels of ALT,AST,TC,TG,MDA contents,and CAT and GSH-Px activity of mice in the model group increased significantly（ P 〈 0. 01）,while the activity of SOD and weight and liver index decreased significantly（ P 〈 0. 01） compared with the normal control group. After 4 weeks of gavage,VCFP could significantly improve weight,liver index and SOD activity,and significantly reduce ALT,AST,TC and TG levels,MDA content and CAT and GSH-Px activity. These results suggest that VCFP can improve antioxidant enzyme activity,remove oxygen free radical and reduce membrane lipid peroxidation reaction,thereby protecting liver cells.

Optimization of Extraction Conditions of Pomegranate Peel Polyphenols and Its Protective Effect on Acute Alcoholic Liver Injury in Mice

[Objectives]This study was conducted to explore the optimization of ultrasonic-assisted organic solvent extraction of pomegranate peel polyphenols(PPPs),and to study the protective effect of PPPs on acute alcoholic liver injury in mice.[Methods]The optimal extraction conditions of PPPs were determined by single factor and orthogonal experiments,and an acute alcoholic liver injury model in mice was established.Bifendate was used as the positive control group to investigate the protective effect of low,medium and high doses of PPPs on acute alcoholic liver injury.[Results]The optimum extraction process parameters were followed as 60%ethanol concentration,solid-liquid ratio of 1:40(w/v),extraction temperature of 50℃,and extraction time of 1.5 h,and the yield was 1.42%.The results of animal experiments showed that PPPs could effectively reduce the degree of alcoholic liver injury in mice,reduce the levels of serum alanine aminotransferase(ALT)and aspartate aminotransferase(AST),and reduce the inflammation and necrosis of liver tissue in mice.Meanwhile,the total polyphenols from pomegranate peel also significantly reduced the expression levels of malondialdehyde(MDA),tumor necrosis factor(TNF-α)and interleukin-6(IL-6)in mice,and increased the levels of superoxide dismutase(SOD)and reduced glutathione(GSH)in liver tissue of mice,indicating its antioxidant and anti-inflammatory effects,further illustrating its protective effect on alcoholic liver injury.[Conclusions]PPPs could reduce the expression levels of TNF-α,IL-6 and MDA in mice,and increase the expression levels of SOD and GSH to achieve the protective effect on acute alcoholic liver injury in mice.This study will provide new ideas for the development of new anti-alcoholic liver injury drug resources.

Risk factors for alcohol-related liver injury in the island population of China: A population-based case-control study

AIM:To investigate the association of alcohol dose, duration of drinking and obesity with abnormal alcohol-related liver injury indicators, the prevalence of alcohol-related liver injury in the island population of China.METHODS:Randomized multistage stratified cluster sampling from the island population of China was used in the population-based case-control study. Then interview, physical examination, laboratory assessments and ultrasonography were done. RESULTS:Daily alcohol intake ≥ 20 g, duration of drinking ≥ 5 years and obesity were closely related to alcohol-related liver injury (P < 0.05). The odds-ratio (OR) (95% CI) was 1.965 (1.122-3.442), 3.412 (1.789-6.507) and 1.887 (1.261-2.824), respectively. The prevalence rate of alcohol-related liver injury in ≥ 20 g daily alcohol intake group and < 20 g daily alcohol intake group was 37.14% and 12.06%, respectively. The prevalence rate of alcohol-related liver injury in ≥ 5 years drinking group and < 5 years drinking group was 34.44% and 8.53%, respectively. No significant dose-response relation was found between daily alcohol intake and abnormal alcohol-related liver injury indicators as well as between duration of drinking and abnormal alcohol-related liver injury indicators. There was no significant difference in the prevalence of alcohol-related liver injury between beer drinking group and yellow rice wine drinking group, hard liquor drinking group, multiple drinking group.CONCLUSION:The risk threshold of daily alcohol intake is 20 g and duration of drinking inducing alcohol-related liver injury 5 years in the island population of China. Liver injury induced by obesity should be concerned.

Complements are involved in alcoholic fatty liver disease, hepatitis and fibrosis

The complement system is a key component of the body's immune system. When abnormally activated, this system can induce inflammation and damage to normal tissues and participate in the development and progression of a variety of diseases. In the past, many scholars believed that alcoholic liver disease(ALD) is induced by the stress of ethanol on liver cells, including oxidative stress and dysfunction of mitochondria and protease bodies, causing hepatocyte injury and apoptosis. Recent studies have shown that complement activation is also involved in the genesis and development of ALD. This review focuses on the roles of complement activation in ALD and of therapeutic intervention in complement-activation pathways. We intend to provide new ideas on the diagnosis and treatment of ALD.

Alcohol use disorder and liver injury related to the COVID-19 pandemic

Alcohol use disorder is a complex and heterogeneous phenomenon that can be studied from several points of view by focusing on its different components.Alcohol is a hepatotoxin whose metabolism creates profound alterations within the hepatocyte.The liver is the central organ in the metabolism of alcohol,a process that also involves other organs and tissues such as the brain,heart and muscles,but the most relevant organ is the liver.The anatomopathological alterations in the liver associated with the prolonged use of alcohol range from the simple accumulation of neutral fats in the hepatocytes,to cirrhosis and hepatocellular carcinoma.Alcohol abuse frequently leads to liver disease such as steatosis,steatohepatitis,fibrosis,cirrhosis,and tumors.Following the spread of coronavirus disease 2019(COVID-19),there was an increase in alcohol consumption,probably linked to the months of lockdown and smart working.It is known that social isolation leads to a considerable increase in stress,and it is also recognized that high levels of stress can result in an increase in alcohol intake.Cirrhotic patients or subjects with liver cancer are immunocompromised,so they may be more exposed to COVID-19 infection with a worse prognosis.This review focuses on the fact that the COVID-19 pandemic has made the emergence of alcohol-induced liver damage a major medical and social problem.

Elevated Linoleic Acid (A Pro-Inflammatory PUFA) and Liver Injury in a Treatment Naive HIV-HCV Co-Infected Alcohol Dependent Patient

HIV and HCV co-infection is a unique disease condition, and medical management of such condition is difficult due to severity and systemic complications. Added with heavy alcohol drinking, risk of liver injury increases due to several pro-inflammatory responses that subsequently get involved with alcohol metabolism. Elevated levels of fatty acids have been reported both in viral infections as well as alcoholic liver disease though such investigations have not addressed the adverse event with dual viral infection of HIV and HCV along with heavy drinking. This case report of a patient with excessive alcohol drinking and first time diagnosis of HIV and HCV dual infection, elaborating concurrent alteration in Linoleic Acid (LA) levels and pro-inflammatory shift in ω-6/ω-3 ratio along with the elevations in liver injury markers. Elevated LA has been recently studied extensively for its role in alcoholic liver disease;and in the present case, we also found it to be clinically relevant to liver injury.

Investigation of paeonol-geniposide on acute alcoholic liver injury based on uniform design method

Objective:To explore the optimal ratio and compatibility effect of paeonol-geniposide combination on acute alcoholic liver injury by uniform design.Methods:Lieber-DeCarli alcoholic liquid feed was used to induce acute alcoholic liver injury in mice.Uniform design was used to select the best dosage combination of paeonol and geniposide,and the related indexes of liver injury and oxidative stress were detected by kit.Serum inflammatory factors were detected by ELISA,and the expressions of p38 MAPK,JNK and NF-κB P65 related proteins in liver were detected by Western-blot.Results:The regression equation suggested that paeonol:geniposide=220:20 was the best ratio of paeonol and geniposide to resist alcoholic liver injury.Compared with the model group,the liver injury indexes and oxidation products of the paeonol+geniposide group decreased significantly,the antioxidant activity of liver tissue increased significantly,and the expression levels of p-p38 MAPK,p-JNK and NF-κB P65 protein decreased significantly.Conclusion:The optimal dosage of paeonolgeniposide was effectively optimized by uniform design and pharmacodynamic analysis.The combination of the two drugs could reduce the alcoholic liver injury by reducing the oxidative stress injury and inflammatory response in the liver tissue of mice,and its effect might be related to the targeting of p38 MAPK/JNK/NF-κB channel.

Betaine inhibits Toll-like receptor 4 expression in rats with ethanol-induced liver injury

AIM:To test whether ethanol feeding could induce Toll-like receptor 4(TLR4)responses,assess the hepatoprotective effect of betaine and its inhibitive effect on TLR4 in animal models of alcoholic liver injury.METHODS:Forty-eight female Sprague-Dawley rats were randomly divided into four groups as control,model,low and high dose betaine groups.Except control group,all rats were fed with high fat-containing diet plus ethanol and fish oil gavages for 8 wk.Betaine was administered intragastrically after exposure of ethanol for 4 wk.The changes of liver histology were examined.The expression of TLR4 mRNA and protein was detected by RT-PCR and Western blotting,respectively.The serum aminotransferase activity alanine transarninase(ALT),aspartate aminotransferase(AST),serum endotoxin,and liver inflammatory factors tumor necrosis factor-α(TNF-α),interferon-γ(IFN-γ),interleukin-18(IL-18)were also assayed.RESULTS:Compared with control group,rats of model group developed marked liver injury,accompanied by an increase of ALT(159.41±7.74 U/L vs 59.47± 2.34 U/L,P<0.0001),AST(248.25±1.40 U/L vs 116.89±3.48 U/L,P<0.0001),endotoxin(135.37± 30.17 ng/L vs 44.15±7.54 ng/L,P<0.0001),TNF-α(20.81±8.58 pg/mL vs 9.34±2.57 pg/mL,P=0.0003),IFN-γ(30.18±7.60 pg/mL vs 16.86±9.49 pg/mL,P= 0.0039)and IL-18(40.99±8.25 pg/mL vs 19.73±9.31 pg/mL,P=0.0001).At the same time,the expression of TLR4 mRNA and protein was markedly induced in the liver after chronic ethanol consumption(1.45±0.07 vs 0.44±0.04,P<0.0001;1.83±0.13 vs 0.56±0.08,P<0.0001).Compared with model group,betaine feeding resulted in significant decreases of ALT(64.93 ±6.06 U/L vs 159.41±7.74 U/L,P<0.0001),AST(188.73±1.11 U/L vs 248.25±1.40 U/L,P<0.0001),endotoxin(61.80±12.56 ng/L vs 135.37±30.17 ng/L,P<0.0001),TNF-α(9.79±1.32 pg/mL vs 20.81± 8.58 pg/mL,P=0.0003),IFN-γ(18.02±5.96 pg/mL vs 30.18±7.60 pg/mL,P=0.0008)and IL-18(18.23±7.01 pg/mL vs 40.99±8.25 pg/mL,P<0.0001).Betaine also improved liver steatosis.The expression levels of TLR4 mRNA or protein in liver tissues were significantly lowered(0.62±0.04 vs 1.45±0.07,P<0.0001;and 0.65±0.06 vs 1.83±0.13,P<0.0001).There was a statistical difference of TLR4 mRNA and protein expression between high-and low-dose betaine groups(0.62±0.04 vs 0.73±0.05,P<0.0001,and 0.65±0.06 vs 0.81±0.09,P<0.0001).CONCLUSION:Betaine can prevent the alcoholinduced liver injury effectively and improve the liver function.The expression of TLR4 increases significantly in ethanol-fed rats and betaine administration can inhibit TLR4 expression.

Epigenetic effects of ethanol on liver and gastrointestinal injury

Alcohol consumption causes cellular injury. Recent developments indicate that ethanol induces epigenetic alterations, particularly acetylation, methylation of histones, and hypo- and hypermethylation of DNA. This has opened up a new area of interest in ethanol research and is providing novel insight into actions of ethanol at the nucleosomal level in relation to gene expression and patho-physiological consequences. The epigenetic effects are mainly attributable to ethanol metabolic stress (Emess), generated by the oxidative and non-oxidative metabolism of ethanol, and dysregulation of methionine metabolism. Epigenetic changes are important in ethanol-induced hepatic steatosis, fibrosis, carcinoma and gastrointestinal injury. This editorial highlights these new advances and its future potential.

Tamarix chinensis Lour inhibits chronic ethanol-induced liver injury in mice

BACKGROUND Tamarix chinensis Lour(TCL)is a shrub that usually grows in arid or semiarid desert areas and saline-alkali fields.It is a traditional Chinese herbal medicine with hepatoprotective,antioxidant,antibacterial,and antitumor activities.AIM To investigate the possible protective effects of TCL against liver injury induced by chronic ethanol intake.METHODS C57BL/6J male mice were fed a Lieber-DeCarli lipid diet containing alcohol and received(by gavage)a water-alcohol extract(80%)of TCL(100 and 200 mg/kg BW)or distilled water for 4 wk.After euthanasia,liver tissues were observed histologically with hematoxylin and eosin staining and Oil red O staining,and the levels of alanine aminotransferase,aspartate transaminase,hepatic lipids,reactive oxygen species,malondialdehyde,and superoxide dismutase were measured.In addition,expression of the NOD-like receptor family,pyrin domain-containing 3(NLRP3)inflammasome and downstream proinflammatory cytokines were determined.RESULTS Compared with the ethanol group,mice in the TCL-treated group(200 mg/kg)had significantly lower serum levels of alanine aminotransferase(mean,34.1 IU/L vs 45.3 IU/L,P<0.01)and aspartate transaminase(mean,89.6 IU/L vs 115.7 IU/L,P<0.01),as well as marked reduction of hepatic tissue reactive oxygen species(decreased by 27.5%,P<0.01)and malondialdehyde(decreased by 76.6%,P<0.01)levels,with a significant increase of superoxide dismutase(Increased by 73.2%,P<0.01).Expression of the NLRP3 inflammasome and its downstream cytokines[interleukin(IL)-1β,tumor necrosis factor-α,and IL-6],and recruitment of natural killer T cells to the liver,were reduced in the TCLtreated incubation with a Lieber-DeCaril ethanol lipid diet group.CONCLUSION These findings suggest that a TCL extract(200 mg/kg)protects against chronic ethanol-induced liver injury,probably by inhibiting the NLRP3-caspase-1-IL-1βsignaling pathway and suppressing oxidative stress.

Chunggan extract, a traditional herbal formula, ameliorated alcohol-induced hepatic injury in rat model

AIM: To evaluate protective effects of Chunggan extract (CGX), a traditional herbal formula, under 4 wk of alcohol consumption-induced liver injury.

Experimental Study of Pratia Extact on Acute Liver Injury in Mice

[Objectives] This study was conducted to observe the protective effect of Pratia extract on acute liver injury in mice.[Methods] Mice were randomly divided into 6 groups according to body weight,10 in each group: normal control group,ethanol-induced/CCl4 liver injury model,low-dose,middle-dose and high-dose Pratia extract groups,and bifendatatum group.Except the blank group,other groups were given 50% ethanol intragastrically at a dose of 12 ml/kg to cause acute alcoholic liver injury,or intraperitoneally injected with 10% CCl4 soybean oil solution to cause acute CCl4 liver injury.The serum ALT and AST activity were measured as well as liver SOD and MDA concentrations.[Results] Pratia extract effectively reduced serum ALT and AST,decreased MDA content and increased liver tissue SOD activity.[Conclusions] Pratia extract has certain protective effect on acute liver injury.

海洋蛋白源解酒护肝水解物的筛选制备及功效评价

以8种海洋生物为原料,通过双酶酶解制备了336种样品,从中筛选出综合效果最好的目标酶解物,海参水解物(Stichopus japonicus peptides,SJPs),即海参先后经过碱性蛋白酶和风味蛋白酶酶解的产物。SJPs拥有较高的体外乙醇脱氢酶激活率(118.86%)、疏水性氨基酸含量(45.97%)、小分子肽含量(81.04%)和胃肠道消化稳定性。建立小鼠急性酒精中毒模型和早期酒精肝病模型,分别评价SJPs解酒和护肝活性。结果表明,饮酒前口服SJPs显著延长小鼠醉酒潜伏期并缩短睡眠期,增强了对急性酒精毒性的耐受性;此外,SJPs通过激活酒精代谢酶系,加速酒精及其代谢物的清除,降低了肝脏氧化应激和脂肪堆积,对早期肝损伤具有显著保护作用。综上所述,SJPs可作为功能食品潜在成分发挥解酒护肝作用。