Abstract Title:

Centella asiatica enhances hepatic antioxidant status and regulates hepatic inflammatory cytokines in type 2 diabetic rats.

Abstract Source:

Pharm Biol. 2017 Dec ;55(1):1671-1678. PMID: 28447512

Abstract Author(s):

Ayodeji B Oyenihi, Novel N Chegou, Oluwafemi O Oguntibeju, Bubuya Masola

Article Affiliation:

Ayodeji B Oyenihi


CONTEXT: Neutralizing the over-activation of oxidative stress and inflammation remains an important goal in the management of type 2 diabetes mellitus (T2DM). Centella asiatica (L.) Urban (Apiaceae) (CA) has been used in traditional folklore in Africa and Asia to treat various ailments including diabetes.

OBJECTIVE: We investigated the hepatic antioxidant and anti-inflammatory potential of methanol extract of CA leaves in T2DM.

MATERIALS AND METHODS: T2DM was induced in male Sprague-Dawley rats with 10% fructose in drinking water for 14 days followed by a single intraperitoneal injection of streptozotocin (40 mg/kg b.wt). Hepatic oxidant/antioxidant status was assessed by measuring the concentrations of malondialdehyde (MDA), ferric reducing antioxidant power (FRAP), oxygen radical absorbance capacity (ORAC), Trolox equivalentantioxidant capacity (TEAC), reduced glutathione (GSH) and activities of glutathione S-transferase (GST) and glutathione peroxidase (GPX). The concentrations of cytokines IL-1β, IL-4, IL-6, IL-10, MCP-1 and TNF-α in the liver were determined.

RESULTS: Diabetes increased MDA formed (47%) and reduced FRAP (20%), TEAC (15%), GSH levels (32%), significantly; decreased GST and GPX activities in the liver and elevated levels of cytokines studied. Treatment of diabetic rats with 500 mg/kg b.wt CA for 14 days decreased MDA (44%); elevated FRAP (15%) and GSH (131%) levels and increased the activities of GST and GPX by 16%. Hepatic concentrations of IL-1β, MCP-1 and TNF-α in DCA group were reduced to 68%, 75% and 63% of DC values, respectively.

CONCLUSIONS: The antioxidant and anti-inflammatory properties of CA may protect tissues such as the liver from diabetes-induced oxidative damage.

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