7 rezultatima
The present study was designed to investigate the effect of embelin in metabolic endotoxemia (ME) mediated inflammation and associated obesity in high fat diet (HFD)-fed C57BL/6 mice. The molecular docking of embelin confirms its binding with the toll-like receptor-4 (TLR-4). In vivo study, mice
Recent studies suggest that Embelin, a natural plant extract might have the potential to prevent body weight gain in rats. However, the mechanisms involved remain to be elucidated.
Effects of Embelin on adipocyte differentiation and lipogenesis were studied in murine ST2 stromal cells and C3H10T1/2
A high-fat diet (HFD) results in hyperlipidemia and an increase in oxidative stress. The purpose of this study was to investigate the preventive effect of embelin against hyperlipidemia and oxidative stress in HFD-induced obesity in rats. Male Wistar rats aged 12 weeks (150-200 g) were fed with an
The embelin derivative 2a was synthesized with the 1,2,3-bistriazole and spectral data confirmed its structural identity. Anti-diabetic and anti-lipidemic effects were evaluated using HFD-STZ induced type 2 diabetic rats. The derivative 2a (30 mg/kg b wt.) supplementation significantly (P ≤ 0.01)
BACKGROUND
The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.
METHODS
Embelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction
Embelia ribes Burm of Myrsinaceae family has been widely used as an herb in the traditional medicine of India. Embelin is an active component extracted from the fruits of Embelia ribes. It has a wide spectrum of biological activities and is not toxic at low dose. This review focuses on the
OBJECTIVE
This paper investigates the hypoglycemic activity of two derivatives of embelin (1) viz. 6-bromoembelin (2) and vilangin (3), in high-fat diet - STZ induced diabetic rats.
METHODS
The effects of 6-bromoembelin (2) and vilangin (3) on insulin resistance, β-cell dysfunction and glucose