Characterisation and Anti-diabetic Activity of Phenylquinoline, and Narceine Isolated from Ficus polita Leaf
A. Nasir, M. S. Sule, A. J. Alhassan, A. M. Wudil, A. A. Imam, A. Idi, I. U. Muhammad, A. I. Yaradua, K. I. Matazu, A. M. Kanadi
Annual Research & Review in Biology · pp. 102–114 · Published 3 Aug 2020
10.9734/arrb/2020/v35i730251Abstract
The present study was conducted to evaluate anti-diabetic potentials of column chromatography fractions (F1-F6) of chloroform leaf extract of Ficus polita and to detect the probable bioactive compounds present in the most active fraction using spectroscopic techniques. Antidiabetic potential of the fractions (F1-F6) were tested at a dose of 50 mg/kg on wistar rats. Fraction 3 and metformin treated diabetic groups showed significant decreases in fasting blood glucose (FBS) level, ameliorate hepatic and renal damages by decreasing the levels of serum total bilirubin, direct bilirubin AST, ALT, creatinine, urea, potassium and chloride, but increasing the levels of serum total protein, albumin, sodium, and bicarbonate compared to untreated diabetic rats. Fraction 3 also stimulates insulin secretion by β cells. After alloxan administration, the levels of hepatic and renal tissues antioxidant markers such as GSH, SOD and catalase were decreased whereas the level of hepatic and renal tissues MDA was elevated. The levels of these antioxidant markers were brought to normalcy by fraction 3 (F3). Histological studies of the pancreas supported the biochemical findings, and treatment with fraction 3 (F3) was found to be effective in restoring alloxan-induced pancreatic toxicity in rats. FTIR and GCMS and analyses were conducted for the detection of bioactive compound(s) in fraction 3 (F3) and the result revealed the presence of "8-methoxy-4-phenylquinoline and narceine The study concludes that; the anti-diabetic property of the leaf of Ficus polita is mediated by the bioactive compounds " 8-methoxy-4-phenylquinoline, and narceine." through their antioxidant properties and stimulation of damaged pancreas to produce more insulin.
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