scholarly journals Rhoifolin Alleviate Alcoholic Liver Disease by Inhibiting the TLR4 / NF-kB Signaling Pathway and Attenuating Oxidative Stress

2021 ◽  
Author(s):  
Baoyu Mai ◽  
Ling Han ◽  
Jiarui Zhong ◽  
Zelin Cao ◽  
Jiaqi Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Hepatic Function ◽  
Flavonoid Compound ◽  
Hepatic Tissue ◽  
Stress Effects ◽  
Excessive Consumption ◽  
Anti Inflammation

Abstract Alcoholic liver disease (ALD) is caused by long-term excessive consumption of alcohol, which is affected by TLR4 / NF-kB mediated inflammatory response and CYP2E1-mediated oxidative stress effects. Rhoifolin (ROF) is a flavonoid compound in Citrus grandis ‘Tomentosa’, with antioxidant and anti-inflammation effect. However, the action of its effect on ALD has been elucidated yet. In the present study, we investigated ROF’s anti-inflammatory, antioxidant and antiapoptotic action in the treatment of ALD. In established ALD mice, ROF promoted hepatic function through downgrading the amount of aminotransferase, attenuating oxidative stress, and restoring antioxidant balance in hepatic tissue. Additionally, ROF significantly reduced the expression of inflammatory cytokines, such as NF-kB, TNF-a, IL-6, and IL-1b in the mice. In vitro experiments indicated that ROF increased the LO2 cells viability and inhibited cells apoptosis. ROF reversed the expression of CYP2E1, NLRP3, p-p65, p-IkB and TLR4, which were consistent with animal experiment. Overall, ROF can alleviate ethanol-induced liver injury through inhibiting oxidative stress and inflammation, and is a promising compound for ALD treatment.

A polysaccharide of PFP-1 from Pleurotus geesteranus attenuates alcoholic liver diseases via Nrf2 and NF-κB signaling pathways

2021 ◽  
Author(s):  
Xinling Song ◽  
Wenxue Sun ◽  
Wenxin Cai ◽  
Le Jia ◽  
Jianjun Zhang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Liver Injury ◽  
Signaling Pathways ◽  
Alcoholic Liver Disease ◽  
Fruiting Body ◽  
Liver Diseases ◽  
Alcoholic Liver Diseases

A polysaccharide named as PFP-1 was isolated from Pleurotus geesteranus fruiting body, and the potential investigations on ameliorating oxidative stress and liver injury against alcoholic liver disease (ALD) were processed...

Long- Term Management Of Alcoholic Liver Disease

2009 ◽  
pp. 159-182
Author(s):  
Craig McClain ◽  
Luis Marsano ◽  
Zhenyuan Song ◽  
Charles Mendenhall ◽  
Marion McClain ◽  
...  
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Term Management

scholarly journals Crosstalk between Oxidative Stress and Inflammatory Liver Injury in the Pathogenesis of Alcoholic Liver Disease

2022 ◽  
Vol 23 (2) ◽  
pp. 774
Author(s):  
Yoon Mee Yang ◽  
Ye Eun Cho ◽  
Seonghwan Hwang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Pathological Features ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol ◽  
The Relationship

Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD.

scholarly journals AN AYURVEDIC MANAGEMENT OF ALCOHOLIC LIVER DISEASE W.S.R TO SHAKHASHRITA KAMALA - A CASE STUDY

2021 ◽  
Vol 9 (11) ◽  
pp. 2870-2876
Author(s):  
Samata Samata ◽  
Shaila Borannavar ◽  
Ananta S Desai
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Pathological Condition ◽  
The Body ◽  
Lower Limbs ◽  
Medical College ◽  
Chief Complaints ◽  
Excessive Consumption ◽  
Bilateral Lower Limb ◽  
Deep Yellow

Alcoholic liver disease is a pathological condition of the liver parenchymal tissue due to excessive consumption of alcohol over a long period of 6-10 years or even earlier. Here in we present a case of a married male of 35 yr. old reported in the Panchakarma OPD of SJIIM Government Ayurveda Medical College Bengaluru on 30th -Jan- 2021, with chief complaints of swelling in the bilateral lower limbs, deep yellowish and burning micturition, yel- lowish discoloration of sclera, reduced appetite, nausea and generalized weakness in the body since 3 months, with the increased level of LFT and USG-abdomen report suggesting hepatomegaly with fatty changes, was ex- amined and diagnosed as alcoholic liver disease and treated with Amapachana with Trikatu Churna, Nitya Virechana with Chitraka Haritaki Leha fallowed by Mustadi Yapana Basti had shown a very good improvement in normalizing appetite, bilateral lower limb swelling and deep yellow micturition. Total bilirubin, SGOT and ALP values were reduced. Keywords: Alcoholic Liver disease, Shakhashrita Kamala, Nitya Virechana

LONG-TERM FOLLOW-UP AFTER LIVER TRANSPLANTATION FOR ALCOHOLIC LIVER DISEASE UNDER TACROLIMUS1

2000 ◽  
Vol 70 (9) ◽  
pp. 1335-1342 ◽  
Author(s):  
Ashok Jain ◽  
Andrea DiMartini ◽  
Randeep Kashyap ◽  
Ada Youk ◽  
Susan Rohal ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Long Term Follow Up

scholarly journals Investigating RNA expression profiles altered by nicotinamide mononucleotide therapy in a chronic model of alcoholic liver disease

2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Mohammed A. Assiri ◽  
Hadi R. Ali ◽  
John O. Marentette ◽  
Youngho Yun ◽  
Juan Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Mapk Pathway ◽  
Early Stage ◽  
Expression Profiles ◽  
Ethanol Metabolism ◽  
Metabolic Dysregulation ◽  
Nicotinamide Mononucleotide ◽  
The Impact

Abstract Background Chronic alcohol consumption is a significant cause of liver disease worldwide. Several biochemical mechanisms have been linked to the initiation and progression of alcoholic liver disease (ALD) such as oxidative stress, inflammation, and metabolic dysregulation, including the disruption of NAD+/NADH. Indeed, an ethanol-mediated reduction in hepatic NAD+ levels is thought to be one factor underlying ethanol-induced steatosis, oxidative stress, steatohepatitis, insulin resistance, and inhibition of gluconeogenesis. Therefore, we applied a NAD+ boosting supplement to investigate alterations in the pathogenesis of early-stage ALD. Methods To examine the impact of NAD+ therapy on the early stages of ALD, we utilized nicotinamide mononucleotide (NMN) at 500 mg/kg intraperitoneal injection every other day, for the duration of a Lieber-DeCarli 6-week chronic ethanol model in mice. Numerous strategies were employed to characterize the effect of NMN therapy, including the integration of RNA-seq, immunoblotting, and metabolomics analysis. Results Our findings reveal that NMN therapy increased hepatic NAD+ levels, prevented an ethanol-induced increase in plasma ALT and AST, and changed the expression of 25% of the genes that were modulated by ethanol metabolism. These genes were associated with a number of pathways including the MAPK pathway. Interestingly, our analysis revealed that NMN treatment normalized Erk1/2 signaling and prevented an induction of Atf3 overexpression. Conclusions These findings reveal previously unreported mechanisms by which NMN supplementation alters hepatic gene expression and protein pathways to impact ethanol hepatotoxicity in an early-stage murine model of ALD. Overall, our data suggest further research is needed to fully characterize treatment paradigms and biochemical implications of NAD+-based interventions.

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