Isolated compounds from Cuscuta pedicellata ameliorate oxidative stress and upregulate expression of some energy regulatory genes in high fat diet induced obesity in rats.

Abstract

Cuscuta pedicellata and some of its isolated compounds were suggested previously to have an anti-obesity effect in rats. This study aimed to investigate the effect of ten isolated compounds from C. pedicellata on insulin resistance, some oxidative stress markers and expression of the mitochondrial uncoupling protein-1 (UCP-1) and Carnitine palmitoyltransferase-I (CPT-1) genes in brown adipose tissue of high fat diet (HFD) rats. One hundred and four male albino rats were divided into 13 groups. Group (1) was considered as normal untreated rats. Obesity was induced in all other groups by HFD. Group (2) served as obese control group and groups (3-11) were treated for four weeks with C. pedicellata extract or one of its isolated compounds (naringenin, kaempferol, aromadenderin, quercetin, 3,5,7,30,50-pentahydroxy flavanone, naringenin-7-O-b-d-glucoside, aromadenderin-7-O-b-d-glucoside, taxifolin 7-O-b-d-glucoside, kaempferol-3-O-b-d-glucoside [astragalin], and quercitin-3-O-b-d-glucoside [isoquercitrin]). At the end of the experiment, rats were then sacrificed under anesthesia and their brown adipose tissues were dissected out for determination of UCP-1 and CPT-1 genes using quantitative PCR. Blood samples were collected for determination of blood glucose, insulin, thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD) and catalase. A significant reduction in homeostasis model assessment-insulin resistance (HOMA-IR) and TBARS levels was observed in rats treated with C. pedicellata crude extract and some of its isolated compounds, with a significant increase in SOD and catalase levels and upregulation of UCP-1 and CPT-1 genes expression compared to the obese control group. This study suggests a beneficiary role of C. pedicellata in reducing insulin resistance, oxidative stress and enhancing energy expenditure.