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Targeting NLRP3 inflammasome via acetylsalicylic acid: Role in suppressing hepatic dysfunction and insulin resistance induced by atorvastatin in naïve versus alcoholic liver in rats.

Authors: El-Kharashi, Omnyah A  El-Din Aly El-Waseef, Dalia Alaa  Nabih, Enas S  Mohamed, Doaa I 
Citation: El-Kharashi OA, etal., Biomed Pharmacother. 2018 Aug 14;107:665-674. doi: 10.1016/j.biopha.2018.08.032.
Pubmed: (View Article at PubMed) PMID:30118883
DOI: Full-text: DOI:10.1016/j.biopha.2018.08.032


BACKGROUND: NLRP3 inflammasome is described in many pathological conditions and is also involved in drug induced liver injury.
AIM OF THE WORK: To investigate the role of NLRP3 inflammasome in liver injury induced by chronic alcohol and/or atorvastatin ingestion.
MATERIALS AND METHODS: Sixty male Wistar rats were used. They were divided into 5 groups: (I) control naïve (II) Alcoholic: given ethanol 8¿g/kg/day, p.o (III) Atorvastatin: given atorvastatin 10¿mg/kg/day, p.o. (IV) Alcoholic¿+¿atorvastatin (V) Acetylsalicylic acid (ASA): given ASA 10¿mg/kg/day, p.o together with alcohol and atorvastatin. Isolated perfused liver, biochemical and histological studies were done.
RESULTS: Atorvastatin and alcohol induced liver inflammation with increasing the expression of NLRP3, IL-1ß and caspase-8 immune-reaction. Atorvastatin and alcohol decreased the reduced form of glutathione in hepatic tissues and induced insulin resistance. ASA administration alleviated the hepatotoxic effects of alcohol and atorvastatin to a significant extent.
CONCLUSIONS: Acetylsalicylic acid alleviated the hepatotoxic effects of alcohol and atorvastatin through decreasing the production of NLRP3 inflammasome in rats' liver.

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RGD Object Information
RGD ID: 13782287
Created: 2018-08-31
Species: All species
Last Modified: 2018-08-31
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.