5‐ALA/SFC Attenuated Binge Alcohol–Induced Gut Leakiness and Inflammatory Liver Disease in HIV Transgenic Rats

Background This study aimed to investigate the protective effect of 5‐aminolevulinic acid (5‐ALA) and sodium ferrous citrate (SFC) against binge alcohol–induced gut leakiness and inflammatory liver disease in HIV transgenic (TG) rats. Methods TG rats were treated with 3 consecutive doses of binge et...

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Published in:Alcoholism, clinical and experimental research clinical and experimental research, 2019-08, Vol.43 (8), p.1651-1661
Main Authors: Liu, Chi, Zhu, Ping, Fujino, Masayuki, Zhu, Shuoji, Ito, Hidenori, Takahashi, Kiwamu, Nakajima, Motowo, Tanaka, Tohru, Zhuang, Jian, Li, Xiao‐Kang
Format: Article
Language:English
Subjects:
5‐aminolevulinic acid
Alanine Transaminase - blood
Alcohol
Alcohol use
Alcoholic beverages
Aminolevulinic acid
Aminolevulinic Acid - pharmacology
Animals
Antigens, CD - biosynthesis
Antigens, CD - immunology
Antigens, Differentiation, Myelomonocytic - biosynthesis
Antigens, Differentiation, Myelomonocytic - immunology
Aspartate Aminotransferases - blood
Binge Alcohol Exposure Liver Injury
Binge Drinking - physiopathology
Cell activation
Cell Adhesion Molecules, Neuronal - genetics
Chemokines
Citric acid
Cytokines
Digestive system
Digestive tract
Endotoxins
Endotoxins - blood
Enterobacteriaceae Infections - microbiology
Ethanol
Ethanol - adverse effects
Exposure
Ferrous Compounds
gag Gene Products, Human Immunodeficiency Virus - genetics
Gene expression
Heme Oxygenase (Decyclizing) - biosynthesis
Heme Oxygenase-1 - biosynthesis
Heme Oxygenase‐1
Hepatitis - blood
Hepatitis - complications
Hepatitis - prevention & control
HIV
HIV Infections - complications
HIV-1 - genetics
Human immunodeficiency virus
Inflammation
Inflammation Mediators - metabolism
Intestine
Intestines - physiopathology
Leptin
Lipopolysaccharides - blood
Liver
Liver - metabolism
Liver diseases
Macrophages
Monocyte chemoattractant protein 1
Permeability - drug effects
Rats
Rats, Transgenic
Receptors, Cell Surface - biosynthesis
Receptors, Cell Surface - immunology
Signal transduction
SIRT1 protein
Sirtuin 1 - biosynthesis
Sodium
Stem Cells
Triglycerides - metabolism
Zonula Occludens-1 Protein - biosynthesis
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Summary:Background This study aimed to investigate the protective effect of 5‐aminolevulinic acid (5‐ALA) and sodium ferrous citrate (SFC) against binge alcohol–induced gut leakiness and inflammatory liver disease in HIV transgenic (TG) rats. Methods TG rats were treated with 3 consecutive doses of binge ethanol (EtOH) with or without 5‐ALA/SFC. Blood and liver tissue samples were collected at 6 hours following the last dose of EtOH. Results Compared with the wild‐type (WT) rats, the TG rats showed increased sensitivity to alcohol‐mediated inflammation, as evidenced by the significantly elevated levels of serum endotoxin, AST, ALT, ED1, and ED2 staining in liver. In contrast, 5‐ALA/SFC improved the above biochemical and histochemical profiles. 5‐ALA/SFC also attenuated the up‐regulated mRNA expression of leptin and CCL2. Furthermore, down‐regulated intestinal ZO‐1 protein expression was also inhibited by 5‐ALA/SFC. Moreover, the expressions of HO‐1, HO‐2, Sirt1, and related signal transduction molecules in liver were increased by 5‐ALA/SFC. These results demonstrated that 5‐ALA/SFC treatment ameliorated binge alcohol exposure liver injury in a rat model of HIV‐infected patients by reducing macrophage activation and expression of inflammatory cytokines/chemokines, and by inducing HO‐1, HO‐2, and Sirt1 expression. Conclusions Taken together, these findings suggested that treatment with 5‐ALA/SFC has a potential therapeutic effect for binge alcohol exposure liver injury in HIV‐infected patients. Protective effect of 5‐ALA and SFC against binge alcohol‐induced gut leakiness and inflammatory liver disease in HIV transgenic rats which are model of HIV‐infected patients was investigated. 5‐ALA/SFC treatment improved biochemical and histochemical profiles, attenuated the up‐regulated mRNA expression of leptin and the downstream target chemokine CCL2, increased the expressions of HO‐1, HO‐2, Sirt1 in liver, and inhibited down‐regulated intestinal ZO‐1 expression. These results suggested a potential therapeutic effect for binge alcohol exposure liver injury in HIV patients.
ISSN:0145-6008
1530-0277
DOI:10.1111/acer.14117