Abstract
Objective Previous studies have characterized the hepatoprotective and anti-inflammatory properties of oleanolic acid (OA). This study aimed to investigate the molecular mechanisms of OA hepatoprotection in concanavalin A- (ConA-) induced acute liver injury. Materials and Methods ConA (20 mg/kg) was intravenously injected to induce acute liver injury in Balb/C mice. OA pretreatment (20, 40, and 80 mg/kg) was administered subcutaneously once daily for 3 consecutive days prior to treatment with ConA; 2, 8, and 24 h after ConA injection, the levels of serum liver enzymes and the histopathology of major factors and inflammatory cytokines were determined. Results OA reduced the release of serum liver enzymes and inflammatory factors and prevented ConA mediated damage to the liver. OA elevated the expression levels of peroxisome proliferator-activated receptor alpha (PPARα) and decreased the phosphorylation of c-Jun NH2-terminal kinase (JNK). Conclusion OA exhibits anti-inflammatory properties during ConA-induced acute liver injury by attenuating apoptosis and autophagy through activation of PPARα and downregulation of JNK signaling.
Highlights
The liver is a metabolic and immunological organ that performs a variety of functions, including deoxidation, glycogen storage, and secretory protein synthesis
concanavalin A- (ConA-)induced liver injury is a well-established model to explore the pathogenesis of liver injury [3,4,5], as it is characterized by elevated liver enzymes and inflammatory cytokines, such as TNF-α, IL-1β, IL-4, and IL-6, leading to the activation of T cells, sinusoidal endothelial cells (SECs), and Kupffer cells (KCs) [3, 6,7,8,9]
Immunohistochemistry analysis and TdT-mediated dUTP nick end labeling (TUNEL) staining confirmed these results (Figures 4(c) and 4(d)). These findings suggest that oleanolic acid (OA) regulates autophagy and apoptosis and protects hepatocytes from pathological damage induced by Concanavalin A (ConA)
Summary
The liver is a metabolic and immunological organ that performs a variety of functions, including deoxidation, glycogen storage, and secretory protein synthesis. Concanavalin A (ConA) is a mitogenic plant lectin extracted from Canavalia brasiliensis [2] that has been used to model liver injury in vivo. ConA-induced liver injury is a well-established model to explore the pathogenesis of liver injury [3,4,5], as it is characterized by elevated liver enzymes and inflammatory cytokines, such as TNF-α, IL-1β, IL-4, and IL-6, leading to the activation of T cells, sinusoidal endothelial cells (SECs), and Kupffer cells (KCs) [3, 6,7,8,9]. Animal studies have shown that apoptosis and autophagy are associated with ConA-induced liver injury in a c-Jun NH2-terminal kinase- (JNK-) dependent manner [10,11,12,13]. Though the exact mechanistic targets modulated by OA during liver injury are unknown, several groups have
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