Ethnopharmacological activity of Hedera nepalensis K. Koch extracts and lupeol against alloxan-induced type I diabetes

Waleed Javed Hashmi,Laila Jafri,Bushra Mirza,Hammad Ismail

doi:10.1590/s2175-97902019000318406

Waleed Javed Hashmi, Laila Jafri + Show 2 more

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https://doi.org/10.1590/s2175-97902019000318406

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Abstract

In this study, we investigated the protective effects of Hedera nepalensis crude extract, its fractions and lupeol in alloxan-induced diabetic rats. Lupeol and n-hexane (HNN) fraction significantly reduced the blood glucose level by increasing insulin level in time dependent manner, and also significantly increased amylase and lipase activity in diabetic rats. Elevated levels of alanine transaminases (ALT), aspartate transaminases (AST), thiobarbituric acid reactive substances (TBARS), nitrite, hydrogen peroxide (H2 O2 ), total bilirubin and total protein in blood serum were efficiently restored to normal levels. Suppressed enzymatic activity of catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and peroxidase (POD) were also restored to their normal levels. Kidney functions were also restored to normal level after treatment with HNN and lupeol. HNN fraction and lupeol of H. nepalensis prevented oxidative stress in alloxan-induced diabetic rats. This study signifies the importance of H. nepalensis and lupeol in ameliorating diabetes by inducing insulin secretion in diabetic model rats.

Highlights

Diabetes Mellitus (DM) is a metabolic disorder characterized by high blood glucose concentration due to insufficient secretion of insulin from pancreatic β-cells (Jarald, Joshi, Jain, 2008)
No mortality was recorded in the experimental animals at any dose from 100 mg/kg BW upto maximum of 1000 mg/kg BW
The crude extract of H. nepalensis produced 55.1% reduction in the blood glucose level of diabetic rats while among the fractions, HNN resulted in 70.0% decrease in the level of blood glucose (Figure 1)

Summary

Introduction

Diabetes Mellitus (DM) is a metabolic disorder characterized by high blood glucose concentration (hyperglycaemia) due to insufficient secretion of insulin from pancreatic β-cells (Jarald, Joshi, Jain, 2008). Glycogen breakdown exacerbates due to low insulin secretion, leading to low hepatic glycogen level. Abnormal glycogen metabolism causes overexpression of the liver marker enzymes: transaminases and phosphatases (Amarapurkar, Das, 2001). Diabetes causes oxidative stress that acts to change cellular physiology, with decreased level of catalase (CAT), renal superoxide dismutase (SOD) and reduced glutathione (GSH) (Tiwari et al, 2013). Oxidative stress has been implicated as major factor leading to pathogenesis and complication of diabetes (Nakhjavani et al, 2013). Liver is the most affected organ in chronic diabetes (Leclercq et al, 2007). About 170 million people are diabetic, and it is estimated that this figure will double by 2030 (Marx, 2002). Development of new therapies to ameliorate DM is a hot research area

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