Alcoholic Liver Damage Research Articles

Clinical formulation Zhigan Oral Liquid intervenes in alcoholic liver injury by regulating the intestinal flora and PI3K\\AKT\\NF-κB pathway

Introduction: Zhigan Oral Liquid (ZOL) was developed from the empirical formulation of Professor Zhao Wenxia, a nationally renowned practitioner of Chinese medicine, and it has been used in Chinese medicine for many years for the effective treatment of alcoholic liver damage (ALD). However, the interventional mechanism of action of the dosage indications for different stages of ALD pathogenesis is not clear. Methods: The main chemical components of ZOL were qualitatively analyzed by ultra-high performance liquid chromatography (UHPLC-Q-Orbitrap HRMS) in tandem with quadrupole electrostatic field orbital well high resolution mass spectrometry and quantitatively analyzed by high-performance liquid chromatography (HPLC). Network pharmacological analysis was performed to predict the targets and pathways of the potential pharmacodynamic components. The pharmacodynamic effects and potential target mechanisms were verified in a murine model of ALD. To observe the effect of ZOL on the intestinal flora, 16s rDNA sequencing was performed on ALD mice. Results: ZOL can achieve alcohol detoxification by increasing the activity of ALDH and other detoxification enzymes and can intervene in the process of alcoholic liver injury and liver fibrosis by regulating the alcohol-induced bacterial dysbiosis, increasing the level of antioxidants, and inhibiting the activation of the PI3K\\AKT\\NF-κB signaling pathway. Kakkalide, Luteolin, Puerarin, tectoridin, and dihydromyricetin are related to the flavonoids that may be the main pharmacodynamic components that exert their medicinal effects. Conclusions: The findings have significant implications for the development of Empirical treatments for alcoholic liver injury. Furthermore, the study contributes to promoting development and utilization of new dosage forms of hospital preparations by emphasizing the composition identification and animal experimental efficacy of ZOL. Overall, this study provides valuable insights into establishing an alcohol-induced liver injury model, and demonstrates the potential of ZOL as a common treatment for alcoholic liver injury a rich source.

Curcumin delivery nanoparticles based on Maillard reaction of Haematococcus pluvialis protein/galactose for alleviating acute alcoholic liver damage

Curcumin delivery nanoparticles based on Maillard reaction of Haematococcus pluvialis protein/galactose for alleviating acute alcoholic liver damage

Efficacy and Safety of BoozLiv™ as an add on therapy in patients with alcoholic liver disease: An open-label, randomized controlled trial

BackgroundAlcoholic Liver Disease (ALD) poses a significant global health threat, contributing to millions of deaths each year. Despite the well-established link between chronic alcohol consumption and liver damage, treatment options remain limited, emphasizing the need for innovative approaches. MethodsAn open-label, randomized controlled trial was conducted in India, involving 68 adult ALD patients over a 12-week period. The patients were randomized into two groups: one receiving standard therapy and the other receiving standard therapy along with BoozLiv™ syrup. Liver function tests, Model for End-Stage Liver Disease (MELD) scores, and safety parameters were assessed at various intervals. ResultsThe study demonstrated that BoozLiv™ syrup, as an add-on therapy, significantly reduced total bilirubin, direct bilirubin, SGOT, SGPT, ALP, and GGT levels compared to standard therapy alone (p ​< ​0.05). The MELD score, indicative of liver function, showed a substantial improvement in the BoozLiv™ group (p ​< ​0.01). Safety analysis revealed that BoozLiv™ was well-tolerated, with only minor adverse effects such as nausea and vomiting reported. ConclusionBoozLiv™ syrup, used in conjunction with standard therapy, showed promising results in improving liver function and reducing liver damage markers in ALD patients. The safety profile was favorable and no patient has withdrawn their consent due to adverse events. Further long-term studies in larger populations are warranted to validate these findings and establish BoozLiv™ as a potential therapeutic option for ALD.

Preparation of Dendrobium officinale Polysaccharide by Lactic Acid Bacterium Fermentation and Its Protective Mechanism against Alcoholic Liver Damage in Mice.

Dendrobium officinale polysaccharide (DP) was prepared with lactic acid bacterium fermentation to overcome the large molecular weight and complex structure of traditional DP for improving its functional activity and application range in this work. The structure was analyzed, and then the functional activity was evaluated using a mouse model of alcoholic liver damage. The monosaccharide compositions were composed of four monosaccharides: arabinose (0.13%), galactose (0.50%), glucose (24.38%), and mannose (74.98%) with a molecular weight of 2.13 kDa. The connection types of glycosidic bonds in fermented D. officinale (KFDP) were →4)-β-D-Manp(1→, →4)-β-Glcp(1→, β-D-Manp(1→, and β-D-Glcp(1→. KFDP exhibited an excellent protective effect on alcoholic-induced liver damage at a dose of 80 mg/kg compared with polysaccharide separated and purified from D. officinale without fermentation (KDP), which increased the activity of GSH, GSH-Px, and GR and decreased the content of MDA, AST, T-AOC, and ALT, as well as regulated the level of IL-6, TNF-α, and IL-1β to maintain the normal functional structure of hepatocytes and retard the apoptosis rate of hepatocytes. The results proved that fermentation degradation is beneficial to improving the biological activity of polysaccharides. The potential mechanism of KFDP in protecting alcoholic liver damage was inhibiting the expression of miRNA-150-5p and targeting to promote the expression of Pik3r1. This study provides an important basis for the development of functional foods.

Effects of fish oil on insulin resistance in the brains of rats with alcoholic liver damage

This study was to examine the effects of fish oil on alcoholic brain damage in rats, focusing on the insulin signaling pathway. Thirty-six male Wistar rats were divided into control (Lieber-DeCarli control liquid diet), CF25 (control diet + 25 % fish oil substitution), CF57 (control diet + 57 % fish oil substitution), E (Lieber-DeCarli ethanol liquid diet), EF25 (ethanol diet + 25 % fish oil substitution), and EF57 (ethanol diet + 57 % fish oil substitution) groups. The behavioral test was also conducted. After 8 weeks, the E group exhibited brain damage, including nuclear-condensed pyramidal cells and positivity for ionized calcium-binding adaptor molecule 1 (Iba-1) antibody. The E group revealed the higher hippocampal insulin receptor substrate-1 (IRS-1) and hypothalamic glycogen synthase kinase 3β (GSK3β), while presented the lower hepatic IRS-1, hippocampal insulin-like growth factor-1 (IGF-1) receptor and glucose transporter 4 (GLUT4). After fish oil substitution, the brain nuclear condensation was attenuated and the hippocampal IRS-1 and hypothalamic GSK3β were significantly decreased.

Lactobacillus rhamnosus NKU FL1-8 Isolated from Infant Feces Ameliorates the Alcoholic Liver Damage by Regulating the Gut Microbiota and Intestinal Barrier in C57BL/6J Mice.

Alcoholic liver damage is caused by long-term or heavy drinking, and it may further progress into alcoholic liver diseases (ALD). Probiotic supplements have been suggested for the prevention or improvement of liver damage. This study was designed to consider the ameliorative effects of Lactobacillus rhamnosus NKU FL1-8 isolated from infant feces against alcoholic liver damage. The mice were gavaged with a 50% ethanol solution and treated with 109 CFU of L. rhamnosus NKU FL1-8 suspension. The factors for liver function, oxidative stress, inflammation, gut microbiota composition, and intestinal barrier integrity were measured. The results showed that L. rhamnosus NKU FL1-8 could decrease the levels of aspartate aminotransferase (AST) to 61% and alanine aminotransferase (ALT) to 50% compared with ethanol given by gavage. It could inhibit the expression level of malondialdehyde (MDA), increase superoxide dismutase (SOD), glutathione (GSH) to relieve oxidative stress, and down-regulate the cytokines to decrease hepatic inflammation. After treatment, the level of triglycerides was reduced, and the expression levels of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) and the peroxisome proliferators-activated receptor-α (PPAR-α) pathway were up-regulated. Additionally, the 16S rRNA sequencing analysis showed that L. rhamnosus NKU FL1-8 increased the relative abundance of Lactobacillus, Ruminococcaceae, etc. At the same time, L. rhamnosus NKU FL1-8 could significantly reduce lipopolysaccharides (LPS) and enhance intestinal tight junction proteins. These results demonstrated that L. rhamnosus NKU FL1-8 could reduce the level of oxidative stress, fat accumulation, and liver inflammation caused by alcohol in the host. The underlying mechanism could be that L. rhamnosus NKU FL1-8 inhibits LPS by regulating the gut microbiota and repairing the intestinal barrier. Thereby, these findings support L. rhamnosus NKU FL1-8 as a potential functional food for the relief of ALD.

Haematococcus pluvialis polysaccharides improve microbiota-driven gut epithelial and vascular barrier and prevent alcoholic steatohepatitis development

Algal polysaccharides possess many biological activities and health benefits, such as antioxidant, anti-tumor, anti-coagulant, and immunomodulatory potential. Gut microbiota has emerged as one of the major contributor in mediating the health benefits of algal polysaccharides. In this study we showed that Haematococcus pluvialis polysaccharides (HPP) decreased serum transaminase levels and hepatic triglyceride content, alleviated inflammation and oxidative stress in the liver of chronic and binge ethanol diet-fed mice. Furthermore, HPP reduced endotoxemia, improved gut microbiota dysbiosis, inhibited epithelial barrier disruption and gut vascular barrier (GVB) damage in ethanol diet-fed mice. Co-housing vehicle-fed mice with HPP-fed mice alleviated ethanol-induced liver damage and endotoxemia. Moreover, fecal microbiota transplantation from HPP-fed mice into antibiotic-induced microbiota-depleted recipients also alleviated ethanol-induced liver injury and improved gut epithelial and vascular barrier. Our study demonstrated that HPP ameliorated ethanol-induced gut epithelial and vascular barrier dysfunction through alteration of gut microbiota, therefore preventing alcoholic liver damage.

Structural characterization of Aspalatus linearis polysaccharide and its improving effect on acute alcoholic liver injury.

Polysaccharides from natural sources can regulate the composition of intestinal flora through the "gut-liver axis" pathway, potentially ameliorating alcoholic liver injury. Aspalathus linearis, also known as rooibos, is one such natural product that has shown promise in this regard. This study looked at the structural properties of A. linearis polysaccharide (ALP) and how well it would work to treat acute alcoholic liver impairment. This study looks at the composition of monosaccharides, functional groups, and molecular weight (Mw) of a newly discovered water-soluble polysaccharide, named ALP. The polysaccharide is composed of pyranose rings, amide groups, and sulfate groups linked by β-glycosidic linkage. It has a relative Mw of 4.30×103kDa and is composed of glucose, rhamnose, and some other monosaccharides. The study found that treating mice with the model of acute alcoholic liver disease with ALP could alleviate pathological symptoms, inhibit the release of inflammatory cytokines, and suppress indicators of oxidative stress. Experiments have shown that different doses of ALP can activate the P4502E1/Keap1-Nrf2-HO-1 signaling pathway. The regulation of inflammatory factors and downstream antioxidant enzymes occurs as a result. Based on these data, it is likely that ALP protects the liver via the "gut-liver axis" pathway by reducing oxidative stress-related damage, inflammation, and alcohol-related alterations to the gut microbiome. The results indicate that ALP mitigates injury caused by oxidative stress, inflammatory responses, and changes in the gut microbiota induced by alcohol through the "gut-liver axis" pathway, which provides protection to the liver. This provides preliminary evidence for the development of related drugs. PRACTICAL APPLICATION: Researchers extracted a polysaccharide from fresh leaves of Auricularia auricula. The polysaccharide was purified and determined to have a predominantly homogeneous molecular weight. An acute alcoholic liver damage mouse model was established, and it was concluded that the polysaccharide could ameliorate liver injury in mice through the "gut-liver axis" pathway. This novel polysaccharide can be used as an additive to develop functional foods with beneficial effects, which can positively impact the daily maintenance of consumers.

Computational identification of potential bioactive compounds from Triphala against alcoholic liver injury by targeting alcohol dehydrogenase.

Alcoholic liver injury resulting from excessive alcohol consumption is a significant social concern. Alcohol dehydrogenase (ADH) plays a critical role in the conversion of alcohol to acetaldehyde, leading to tissue damage. The management of alcoholic liver injury encompasses nutritional support and, in severe cases liver transplantation, but potential adverse effects exist, and effective medications are currently unavailable. Natural products with their potential benefits and historical use in traditional medicine emerge as promising alternatives. Triphala, a traditional polyherbal formula demonstrates beneficial effects in addressing diverse health concerns, with a notable impact on treating alcoholic liver damage through enhanced liver metabolism. The present study aims to identify potential active phytocompounds in Triphala targeting ADH to prevent alcoholic liver injury. Screening 119 phytocompounds from the Triphala formulation revealed 62 of them showing binding affinity to the active site of the ADH1B protein. Promising lipid-like molecule from Terminalia bellirica, (4aS, 6aR, 6aR, 6bR, 7R, 8aR, 9R, 10R, 11R, 12aR, 14bS)-7, 10, 11-trihydroxy-9-(hydroxymethyl)-2, 2, 6a, 6b, 9, 12a-hexamethyl-1, 3, 4, 5, 6, 6a, 7, 8, 8a, 10, 11, 12, 13, 14b-tetradecahydropicene-4a-carboxylic acid showed high binding efficiency to a competitive ADH inhibitor, 4-Methylpyrazole. Pharmacokinetic analysis further confirmed the drug-likeness and non-hepatotoxicity of the top-ranked compound. Molecular dynamics simulation and MM-PBSA studies revealed the stability of the docked complexes with minimal fluctuation and consistency of the hydrogen bonds throughout the simulation. Together, computational investigations suggest that (4aS, 6aR, 6aR, 6bR, 7R, 8aR, 9R, 10R, 11R, 12aR, 14bS)-7, 10, 11-trihydroxy-9-(hydroxymethyl)-2, 2, 6a, 6b, 9, 12a-hexamethyl-1, 3, 4, 5, 6, 6a, 7, 8, 8a, 10, 11, 12, 13, 14b-tetradecahydropicene-4a-carboxylic acid from the Triphala formulation holds promise as an ADH inhibitor, suggesting an alternative therapy for alcoholic liver injury.

Fucoidan from Apostichopus japonicus ameliorates alcoholic liver disease by regulating gut-liver axis homeostasis

Long-term and excessive alcohol consumption can lead to the development of alcoholic liver disease (ALD), characterized by oxidative damage, intestinal barrier injury, and disruption of intestinal microbiota. In this study, we extracted fucoidan (Aj-FUC) from Apostichopus japonicus using enzymatic methods and characterized its structure. The ALD model was established in male Balb/c mice using 56° Baijiu, with silymarin as a positive control. Mice were orally administered 100 mg/kg·bw and 300 mg/kg·bw of Aj-FUC for 28 days to evaluate its effects on liver injury in ALD mice and explore its potential role in modulating the gut-liver axis. The results showed significant improvements in histopathological changes and liver disease in the Aj-FUC group. Aj-FUC treatment significantly increased the levels of glutathione (GSH) and glutathione peroxidase (GSH-Px) while weakly reduced the elevation of malondialdehyde (MDA) induced by ALD. It also regulated the Nrf2/HO-1 signaling pathway, collectively alleviating hepatic oxidative stress. Aj-FUC intervention upregulated the expression of ZO-1 and Occludin, thus contributing to repair the intestinal barrier. Additionally, Aj-FUC increased the content of short-chain fatty acids (SCFAs) and regulated the imbalance in gut microbiota. These results suggested that Aj-FUC alleviates ALD by modulating the gut-liver axis homeostasis. It may prove to be a useful dietary supplement in the treatment of alcoholic liver damage.

Metallofullerenol alleviates alcoholic liver damage via ROS clearance under static magnetic and electric fields

Alcoholic liver disease (ALD) is a common chronic redox disease caused by increased alcohol consumption. Abstinence is a major challenge for people with alcohol dependence, and approved drugs have limited efficacy. Therefore, this study aimed to explore a new treatment strategy for ALD using ferroferric oxide endohedral fullerenol (Fe3O4@C60(OH)n) in combination with static magnetic and electric fields (sBE). The primary hepatocytes of 8–9-week-old female BALB/c mice were used to evaluate the efficacy of the proposed combination treatment. A mouse chronic binge ethanol feeding model was established to determine the alleviatory effect of Fe3O4@C60(OH)n on liver injury under sBE exposure. Furthermore, the ability of Fe3O4@C60(OH)n to eliminate •OH was evaluated. Alcohol-induced hepatocyte and mitochondrial damage were reversed in vitro. Additionally, the combination therapy reduced liver damage, alleviated oxidative stress by improving antioxidant levels, and effectively inhibited liver lipid accumulation in animal experiments. Here, we used a combination of magnetic derivatives of fullerenol and sBE to further improve the ROS clearance rate, thereby alleviating ALD. The developed combination treatment may effectively improve alcohol-induced liver damage and maintain redox balance without apparent toxicity, thereby enhancing therapy aimed at ALD and other redox diseases.

Soybean meal peptide Gly-Thr-Tyr-Trp could protect mice from acute alcoholic liver damage: A study of protein-protein interaction and proteomic analysis

Alcoholic liver disease (ALD) is a serious health threat. Soybean meal peptide (SMP) supplementation may protect against this damage; however, the potential mechanism underlying the specific sequence of SMPs is unclear. Protein-protein interaction and proteomic analyses are effective methods for studying functional ingredients in diseases. This study aimed to investigate the potential mechanism of action of the peptide Gly-Thr-Tyr-Trp (GTYW) on ALD using protein-protein interaction and proteomic analyses. These results demonstrate that GTYW influenced the targets of glutathione metabolism (glutathione-disulfide reductase, glutathione S-transferase pi 1, and glutathione S-transferase mu 2). It also regulated the expression of targets related to energy metabolism and amino acid conversion (trypsin-2, cysteine dioxygenase type-1, and F6SJM7). Amino acid and lipid metabolisms were identified based on Gene Ontology annotation. These results indicate that GTYW might affect alcohol-related liver disease signaling pathways. This study provides evidence of the protective and nutritional benefits of SMPs in ALD treatment.

ERRγ-inducible FGF23 promotes alcoholic liver injury through enhancing CYP2E1 mediated hepatic oxidative stress

Fibroblast growth factor 23 (FGF23) is a member of endocrine FGF family, along with FGF15/19 and FGF21. Recent reports showed that under pathological conditions, liver produces FGF23, although the role of hepatic FGF23 remains nebulous. Here, we investigated the role of hepatic FGF23 in alcoholic liver disease (ALD) and delineated the underlying molecular mechanism. FGF23 expression was compared in livers from alcoholic hepatitis patients and healthy controls. The role of FGF23 was examined in hepatocyte-specific knock-out (LKO) mice of cannabinoid receptor type 1 (CB1R), estrogen related receptor γ (ERRγ), or FGF23. Animals were fed with an alcohol-containing liquid diet alone or in combination with ERRγ inverse agonist. FGF23 is mainly expressed in hepatocytes in the human liver, and it is upregulated in ALD patients. In mice, chronic alcohol feeding leads to liver damage and induced FGF23 in liver, but not in other organs. FGF23 is transcriptionally regulated by ERRγ in response to alcohol-mediated activation of the CB1R. Alcohol induced upregulation of hepatic FGF23 and plasma FGF23 levels is lost in ERRγ-LKO mice, and an inverse agonist mediated inhibition of ERRγ transactivation significantly improved alcoholic liver damage. Moreover, hepatic CYP2E1 induction in response to alcohol is FGF23 dependent. In line, FGF23-LKO mice display decreased hepatic CYP2E1 expression and improved ALD through reduced hepatocyte apoptosis and oxidative stress. We recognized CBIR-ERRγ-FGF23 axis in facilitating ALD pathology through hepatic CYP2E1 induction. Thus, we propose FGF23 as a potential therapeutic target to treat ALD.

Recent Progresses on Pathophysiology, Diagnosis, Therapeutic Modalities, and Management of Non-alcoholic Fatty Liver Disorder

Abstract: Non-alcoholic fatty liver disease (NAFLD) is currently the utmost common chronic liver disorder that happens through all age groups and is identified to occur in 14%-30% of the general population, demonstrating a critical and grossing clinical issue because of the growing incidence of obesity and overweight. From the histological aspect, it looks like alcoholic liver damage, but it happens in patients who avoid remarkable alcohol usage. NAFLD comprises a broad spectrum, ranging from benign hepatocellular steatosis to inflammatory nonalcoholic steatohepatitis (NASH), different levels of fibrosis, and cirrhosis. Patients with NASH are more susceptible to more rapid progression to cirrhosis and hepatocellular carcinoma. There is no single factor that drives proceeding from simple steatosis to NASH. However, a combination of multi parameters such as genetic background, gut microflora, intake of high fat/ fructose dietary contents or methionine/choline-deficient diet, and consequently accumulated hepatocellular lipids mainly including triglycerides and also other bio-analytes, such as free fatty acids, cholesterol, and phospholipids display a crucial role in disease promotion. NAFLD is related to overweight and insulin resistance (IR) and is regarded as the hepatic presentation of the metabolic syndrome, an amalgamation of medical statuses such as hyperlipidemia, hypertension, type 2 diabetes, and visceral obesity. Despite the increasing prevalence of this disease, which imposes a remarkable clinical burden, most affected patients remain undiagnosed in a timely manner, largely related to the asymptomatic entity of NAFLD patients and the unavailability of accurate and efficient noninvasive diagnostic tests. However, liver biopsy is considered a gold standard for NAFLD diagnosis, but due to being expensive and invasiveness is inappropriate for periodic disease screening. Some noninvasive monitoring approaches have been established recently for NAFLD assessment. In addition to the problem of correct disease course prediction, no effective therapeutic modalities are approved for disease treatment. Imaging techniques can commonly validate the screening and discrimination of NAFLD; nevertheless, staging the disease needs a liver biopsy. The present therapeutic approaches depend on weight loss, sports activities, and dietary modifications, although different insulin-sensitizing drugs, antioxidants, and therapeutic agents seem hopeful. This review aims to focus on the current knowledge concerning epidemiology, pathogenesis, and different biochemical experiments and imaging modalities applied to diagnose the different grades of NAFLD and its management, as well as new data about pharmacological therapies for this disorder.

Alcoholic Hepatitis

Alcoholic hepatitis is a serious liver condition characterized by inflammation and liver damage caused by excessive alcohol consumption. This condition represents a significant health concern worldwide as it can progress to more severe liver diseases, including cirrhosis and liver failure. This abstract provides an overview of alcoholic hepatitis, including its causes, symptoms, diagnosis, and treatment. Long-term alcohol consumption is the primary cause of alcoholic hepatitis. When alcohol is metabolized in the liver, it generates toxic byproducts that can lead to inflammation and cellular damage. Over time, repeated episodes of damage can result in alcoholic hepatitis. Patients with this condition may present with various symptoms including jaundice, abdominal pain, nausea, vomiting, fever, and an enlarged liver. Diagnosis of alcoholic hepatitis typically involves a combination of medical history assessment, physical examination, blood tests, and imaging studies. Elevated levels of liver enzymes, such as AST and ALT, are common laboratory findings. A liver biopsy may be required to confirm the diagnosis and assess the extent of liver damage. Treatment of alcoholic hepatitis primarily focuses on alcohol cessation, which is essential to prevent further liver damage and improve the chances of recovery. Supportive care, such as nutritional supplementation and the management of complications, is also essential. Hospitalization may be necessary for severe cases. The prognosis varies depending on the severity of the condition and the patient's response to treatment. Complete abstinence from alcohol significantly improves the chances of recovery; however, some individuals may progress to advanced liver disease or even liver failure. Liver transplantation may be considered for those with end-stage liver disease. key words Alcoholic hepatitis Liver inflammation Excessive alcohol consumption Liver damage Cirrhosis Liver failure Symptoms Jaundice Abdominal pain Nausea Vomiting Fever Enlarged liver Diagnosis Liver enzymes AST (Aspartate Aminotransferase) ALT (Alanine Aminotransferase) Liver biopsy Treatment Alcohol cessation.

Combined hepatoprotective therapy for experimental alcoholic liver damage

Combined hepatoprotective therapy for experimental alcoholic liver damage

NON-ALCOHOLIC FATTY LIVER DISEASE IN PROCEEDINGS OF CONGRESS EASL – 2023

Background. The significant increase in the prevalence of type 2 diabetes has led to an increase in the incidence of its hepatic manifestations, in particular non-alcoholic fatty liver disease. A complication of this disease is the asymptomatic progression of fibrosis, the development of liver cirrhosis and hepatocellular carcinoma.&#x0D; Aim. To analyze the results of studies on non-alcoholic fatty liver disease that were reviewed at the Congress of the European Association for the Study of the Liver (EASL - 2023).&#x0D; Materials and methods. Analysis of current data presented in the materials of the Congress of the European Association for the Study of the Liver (EASL - 2023) on the prevalence, pathogenesis and treatment of non-alcoholic fatty liver disease.&#x0D; Conclution. Non-alcoholic fatty liver disease and the new term metabolic associated steatohepatitis (MASH) are the hepatic manifestations of type 2 diabetes mellitus, the prevalence of which is rapidly increasing with the increasing incidence of uncontrolled hyperglycemia. The new term MASH, which replaced the diagnosis of NAFLD, emphasizes that the main etiopathogenetic factor in the development of this liver pathology is type 2 diabetes mellitus. The progression of liver fibrosis and the development of hepatocellular carcinoma in MASH can be caused not only by a high level of glycated hemoglobin, but also by multiple comorbid factors, in particular, autoimmune hepatitis, alcoholic and drug-induced liver damage, hemochromatosis, etc.

A review: Alcoholic liver disease pathophysiology, current molecular and clinical perspectives

Alcohol-related liver damage (ALD) is a term used for a variety of liver conditions comprising cirrhosis, fibrosis, and steatohepatitis with chronic inflammation that is predominantly brought on by heavy alcohol consumption. ALD is currently regarded as one of the most common causes of liver disease-related mortality on a global scale. The majority of cirrhosis in the liver cases seen in district general hospitals in the UK are caused by alcohol, which is a key factor in the Western world. Alcoholic cirrhosis, acute alcoholic hepatitis, and alcoholic fatty liver (steatosis) are the three most widely recognized types of alcoholic liver disease. According to the National Institute on Alcohol Abuse and Alcoholism's the most recent surveillance report, liver cirrhosis was among the top twelve causes of death in the country, contributing to a total of 14,477 deaths in the year 2014.This page speaks about the various types of alcoholic liver damage (ALD), with a focus on cirrhosis because it is the type of liver diseases that is most frequently linked to alcohol misuse and has the most studies investigating it. Epidemiological studies have assessed the incidence of ALD and the factors who frequently cause the condition. Although excessive alcohol use is the main cause of ALD, gender and cultural variations also have a significant role in the prevalence of liver disease. Since the 1970s, cirrhosis-related mortality rates have decreased in the United States and certain other countries as well. This dip may have been caused by a variety of variables, including increasing enrollment in alcohol rehab facilities and in Alcoholics Anonymous, drops in alcohol consumption, and more

Pharmacological correction of neurological disorders in the relief of alcohol withdrawal syndrome

Among the existing addictions, the greatest medical and social problems are created by chemical dependencies associated with the use of alcohol, narcotic drugs and psychotropic substances. Neurological disorders in alcoholism are distinguished by the multifactorial nature of their genesis. Pharmacological correction of potential neurological disorders in alcohol users should be considered from the perspective of prescribing drugs with polymodal effects, which justifies the search for the most promising and effective means of pharmacological correction of mental and somatoneurological consequences of alcoholism. The aim of the study was to analyze the dynamics of neurological symptoms under the control of laboratory indicators of toxic liver damage to assess the effectiveness of complex pharmacotherapy of alcohol withdrawal syndrome. 40 patients (average age 43.2±7.2 years) who are being treated for alcohol withdrawal syndrome were examined. A neurological examination and a study of blood biochemical parameters were carried out to assess the functional state of the liver. Neurological organic symptom complex was detected in all observed patients and was a diffuse focal symptomatology associated with cerebral and polyneuritic disorders. Laboratory indicators of the functional state of the liver in patients taking morpholinium- methyl-triazolyl-thioacetate orally showed a statistically significant difference before and after therapy, in the absolute majority of cases positive hemodynamic dynamics and regression of neurological symptoms were observed. Morpholinium-methyl-triazolyl-thioacetate has polymodal effects and can be used not only for alcoholic hepatitis, but also for the correction of cardiological and neurological disorders associated with alcoholic liver damage. It is advisable to consider Thiotriazoline® as a means of choice in the complex therapy of alcoholic liver damage in the outpatient unit.

Progress in the mechanism of autophagy and traditional Chinese medicine herb involved in alcohol-related liver disease.

Alcohol-related liver disease (ALD) is chronic liver damage caused by long-term heavy drinking with, extremely complicated pathogenesis. The current studies speculated that excessive alcohol and its metabolites are the major causes of liver cell toxicity. Autophagy is evolutionarily conserved in eukaryotes and aggravates alcoholic liver damage, through various mechanisms, such as cellular oxidative stress, inflammation, mitochondrial damage and lipid metabolism disorders. Therefore, autophagy plays an critical role in the occurrence and development of ALD. Some studies have shown that traditional Chinese medicine extracts improve the histological characteristics of ALD, as reflected in the improvement of oxidative stress and lipid droplet clearance, which might be achieved by inducing autophagy. This article reviews the mechanisms of quercetin, baicalin, glycycoumarin, salvianolic acid A, resveratrol, ginsenoside rg1, and dihydromyricetin inducing autophagy and their participation in the inhibition of ALD. The regulation of autophagy in ALD by these traditional Chinese medicine extracts provides novel ideas for the treatment of the disease; however, its molecular mechanism needs to be elucidated further.