Oleuropein protects against lipopolysaccharide‐induced sepsis and alleviates inflammatory responses in mice

Abstract

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.

Protocatechuic acid attenuates lipopolysaccharide‐induced septic lung injury in mice: The possible role through suppressing oxidative stress, inflammation and apoptosis

“…injected with a single dose of LPS (10 mg/kg b.w.) dissolved in endotoxin-free saline (Alsharif et al, 2020); Group 4, 5, and 6 (PCA10-LPS, PCA20-LPS, and PCA30-LPS groups, respectively) mice were orally administered PCA at doses of 10 (low dose), 20 (average dose), and 30 (high dose) mg/kg b.w., respectively, for seven days followed by LPS injection as previously described.…”

“…Sepsis is considered a life-threatening and serious illness syndrome that occurs due to dysregulation of the host response to infection (Alsharif et al, 2020). Epidemiological studies have shown that septic shock and multiple organ dysfunction syndromes are the main causes of death in half or more of the patients in intensive care unit (Mutlu & Budinger, 2006).…”

Astaxanthin Protects Dendritic Cells from Lipopolysaccharide-Induced Immune Dysfunction

“…For instance, single cytokine, or a combination of multiple cytokines, including G-CSF, GM-CSF, IFN-γ, IL-3, IL-7, and IL-15, were introduced into sepsis therapy, according to a disease-specific progression and patient immune responses [ 8 ]. Some immunosuppressive agents, such as bursopentin [ 9 ], curcumin [ 10 ], and oleuropein [ 11 ], provided protection against inflammatory injury in the LPS-induced sepsis models.…”

Serum proteins may facilitate the identification of Kawasaki disease and promote in vitro neutrophil infiltration

“…Lipopolysaccharide (LPS) is usually applied in animal model to induce systemic inflammation 46,47 and also applied in leukocytes or other cells to induce inflammatory reactions or cell damage 48,49 . However, LPS is seldom applied in neutrophils to examine transendothelial migration.…”