Premium
Oleuropein protects against lipopolysaccharide‐induced sepsis and alleviates inflammatory responses in mice
Author(s) -
Alsharif Khalaf F.,
Almalki Abdulraheem A.,
AlAmer Osama,
Mufti Ahmad H.,
Theyab Abdulrahman,
Lokman Maha S.,
Ramadan Shimaa S.,
Almeer Rafa S.,
Hafez Mohamed M.,
Kassab Rami B.,
Abdel Moneim Ahmed E.
Publication year - 2020
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2347
Subject(s) - lipopolysaccharide , sepsis , medicine , kidney , proinflammatory cytokine , creatinine , pharmacology , inflammation , intraperitoneal injection , acute kidney injury , blood urea nitrogen , oleuropein , lactate dehydrogenase , immunology , endocrinology , chemistry , antioxidant , biochemistry , enzyme
Sepsis results from a major systemic inflammatory response and can induce disorders in multiple organs. The present study evaluated the potential protective effects of oleuropein (OLE) against hyperinflammatory responses during lipopolysaccharide (LPS)‐induced sepsis in mice. Sixty male Balb/c mice were randomly categorized into five groups of 12 animals each: control, intraperitoneally injected with OLE (50 mg/kg), injected with LPS (10 mg/kg, intraperitoneal), and two groups administered OLE (25 and 50 mg/kg) for 3 days prior to LPS injection. Twenty‐four hours after lipopolysaccharide injection, the animals were sacrificed. Serum, liver, and kidney tissue samples were collected for biochemical analyses, histopathological examinations, and investigation of inflammation‐related gene expression. OLE pretreatment significantly reduced liver damage parameters (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase) and kidney damage parameters (blood urea nitrogen, creatinine, and kidney injury molecule‐1) in the septic mice. OLE pretreatment ameliorated LPS‐induced liver and kidney histological changes. OLE significantly mitigated the increased levels of malondialdehyde in the liver and kidneys and reduced levels of reduced glutathione induced by LPS. LPS injection also resulted in increased expression of the proinflammatory cytokines (TNF‐α, IL‐1β, and IL‐6) and inflammation‐related genes ( Nos2 , Hmgb1 , Mpo , Cd46 , Map2k4 , and Map2k7 ) in the hepatic and renal tissues. OLE reduced these expressions to ameliorate the inflammatory response. Moreover, OLE pretreatment enhanced the survival rate of septic mice. In conclusion, OLE alleviated the inflammatory response to protect against LPS‐induced sepsis in mice.