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The Role of LVV-H7 in Alcohol-Induced Reward Mechanisms

ABSTRACT: Hemorphins are short peptides generated during cleavage of the hemoglobin chains but alpha chain, with various functions in different systems and tissues in both physiology and pathophysiology. The main purpose of this study was to establish the role of LVV-H7 in the mechanism of alcohol dependence. LVV-hemorphin 7 (LVV-H7) is released at higher concentrations in the presence of alcohol in vitro. Therefore, we predicted that alcohol intake can change the level of LVV-H7. We have accomplished behavioral tests in animal studies, along with proteomic analysis of the CNS tissues of alcohol addicted rats to verify the correlation of LVV-H7 level and ethanol dependence. We have also confirmed the BBB permeability of synthesized LVV-H7, as well as an inhibitor of its releasing enzyme- pepstatin using fluorescent microscopy. We have found a dose-dependent correlation between LVV-H7 and the time spent by rats in the drug-associated compartment using CPP test. Utilizing mass spectrometry-based methods we identified protein binding targets of LVV-H7 in the CNS tissue of addicted rats, along with the LVV-H7 degrading enzymes. The interpretation of the obtained results reveals the substantial role of LVV-H7 in the mechanism of alcohol dependence.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Brain

DISEASE(S): Alcohol Dependence

SUBMITTER: Przemyslaw Mielczarek

LAB HEAD: Przemyslaw Mielczarek

PROVIDER: PXD036448 | Pride | 2025-09-05

REPOSITORIES: Pride

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Project description:The etiology of alcohol dependence is not completely understood. Increasing evidence reveals that gut microbiota dysbiosis is associated with certain psychiatric disorders, including alcoholism, through the 'microbiota-gut-brain' axis. The aims were to evaluate the effect of alcohol abuse on the gut microbiota, intestinal permeability and serum metabolic profile and to determine whether alcohol-induced alterations in gut microbiota are correlated with gut permeability and serum metabolic phenotype changes. 16S rRNA gene high-throughput sequencing and nontarget metabolomics techniques were applied in an alcohol-dependent rat model in the present study. The results showed that alcohol intake altered the composition and structure of the colonic microbiota, especially the relative abundance of the commensal microbes Lachnospiraceae and Prevotellaceae, which was significantly decreased. Alcohol-dependent rats developed gut leakiness and a serum metabolic phenotype disorder. The valine, leucine and isoleucine biosynthesis pathways and arginine and proline metabolism pathways were obviously influenced by alcohol intake. Moreover, alcohol consumption disturbed the brain's neurotransmitter homeostasis. The regression analysis showed that alcohol-induced colonic microbiota dysbiosis was strongly associated with increased intestinal permeability and serum metabolic phenotype and neurotransmitter disorders. These results revealed that gut microbiota dysbiosis and serum metabolites alteration might be a cofactor for developing of alcohol dependence. IMPORTANCE The gut microbiota dysbiosis is associated with certain psychiatric disorders through the 'microbiota-gut-brain' axis. Here we revealed that alcohol consumption induced the colonic microbiota dysbiosis, increased intestinal permeability, altered the serum metabolic phenotype in rats, and there were a strong correlation between gut microbiota dysbiosis and serum metabolites disorders. Thus, gut microbiota dysbiosis and serum metabolites alteration may be a cofactor for development of alcohol dependence.

			Action	DRS
	F003423.dat	Other
	F003423.mgf	Mgf
	F003424.dat	Other
	F003424.mgf	Mgf
	F003425.dat	Other

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The Role of LVV-H7 in Alcohol-Induced Reward Mechanisms

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