Abstract

BackgroundTherapeutic potential of Prosopis cineraria has been extensively explored by many eminent researchers against various serious diseases but its activity against Lipopolysaccharide (endotoxin) is obscure. Therefore, present experimental investigation was conducted to unravel and analyze the anti-inflammatory potential of hydro-ethanol extract of Prosopis cineraria against LPS-induced inflammation in Swiss albino male mice.MethodsSwiss Albino male mice were intoxicated (intra-peritoneal) with LPS (2 mg/kg body weight) and further treated with low and high dose (i.e. 100 mg/kg body weight and 300 mg/kg body weight respectively) of hydro-ethanol extract of stem-bark of Prosopis cineraria. The levels of cytokines (TNF-α, Prostaglandins E2, IL-6, NF-κBp65, IFN-γ and IL-10) were determined in liver homogenate. Nitric oxide generated due to LPS-induced toxicity was estimated by using Griess reagent.ResultsThe results demonstrated that the plant extract suppressed the over-expression and altered levels of cytokines due to LPS intoxication and restored the levels of TNF-α, NF-κB, NO, IL-6, IFN- γ, Prostaglandin E2 and IL-10.ConclusionThe present research work unravelled the alleviating potential of Prosopis cineraria against LPS-induced inflammation by modulating the expression of cytokines.

Highlights

  • Therapeutic potential of Prosopis cineraria has been extensively explored by many eminent researchers against various serious diseases but its activity against Lipopolysaccharide is obscure

  • The results revealed a novel role in inhibition of inflammatory diseases by lowering the production of Tumour Necrosis Factor α (TNF-α) and IL-6 [13]

  • In the results it was observed that LPS caused elevation in the levels of TNF-α (Fig. 1a), Prostaglandin E2 (Fig. 1b), IL-6 (Fig. 1c) and IFN-γ (Fig. 1d) in LPS-intoxicated group in comparison to untreated group

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Summary

Introduction

Therapeutic potential of Prosopis cineraria has been extensively explored by many eminent researchers against various serious diseases but its activity against Lipopolysaccharide (endotoxin) is obscure. Lipopolysaccharides (LPS), referred as endotoxins, present in the outer monolayer of most gram negative bacteria is known to trigger innate immune response and inflammatory cascade in the host. Excessive and prolonged inflammatory response triggered by LPS in the host can lead to vascular leakage, septic shock or endotoxin shock, tissue and organ damage and can eventually cause death [1]. Studies indicate the massive generation of reactive oxygen species (ROS) in LPS-induced signalling cascade [4]. ROS are known to have biocidal effects on invading micro-organisms and are important components of innate immune response. Generation of ROS can potentially harm the tissues and organs of the host [5, 6].

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