A Novel Triterpenoid Isolated from the Root Bark of Ailanthus excelsa Roxb (Tree of Heaven), AECHL-1 as a Potential Anti-Cancer Agent

We report here the isolation and characterization of a new compound Ailanthus excelsa chloroform extract-1 (AECHL-1) (C(29)H(36)O(10); molecular weight 543.8) from the root bark of Ailanthus excelsa Roxb. The compound possesses anti-cancer activity against a variety of cancer cell lines of different origin.AECHL-1 treatment for 12 to 48 hr inhibited cell proliferation and induced death in B16F10, MDA-MB-231, MCF-7, and PC3 cells with minimum growth inhibition in normal HEK 293. The antitumor effect of AECHL-1 was comparable with that of the conventional antitumor drugs paclitaxel and cisplatin. AECHL-1-induced growth inhibition was associated with S/G(2)-M arrests in MDA-MB-231, MCF-7, and PC3 cells and a G(1) arrest in B16F10 cells. We observed microtubule disruption in MCF-7 cells treated with AECHL-1 in vitro. Compared with control, subcutaneous injection of AECHL-1 to the sites of tumor of mouse melanoma B16F10 implanted in C57BL/6 mice and human breast cancer MCF-7 cells in athymic nude mice resulted in significant decrease in tumor volume. In B16F10 tumors, AECHL-1 at 50 microg/mouse/day dose for 15 days resulted in increased expression of tumor suppressor proteins P53/p21, reduction in the expression of the oncogene c-Myc, and downregulation of cyclin D1 and cdk4. Additionally, AECHL-1 treatment resulted in the phosphorylation of p53 at serine 15 in B16F10 tumors, which seems to exhibit p53-dependent growth inhibitory responses.The present data demonstrate the activity of a triterpenoid AECHL-1 which possess a broad spectrum of activity against cancer cells. We propose here that AECHL-1 is a futuristic anti-cancer drug whose therapeutic potential needs to be widely explored for chemotherapy against cancer

Bitter melon (Momordica charantia) reduces adiposity, lowers serum insulin and normalizes glucose tolerance in rats fed a high fat diet

Bitter melon (BM) is known for its hypoglycemic effect but its effect on rats fed a hyperinsulinemic high fat diet has not been examined. In a dose-response (0.375, 0.75 and 1.5%) study, oral glucose tolerance was improved in rats fed a high fat (HF; 30%) diet supplemented with freeze-dried BM juice at a dose of 0.75% or higher (P < 0.05). At the highest dose, BM-supplemented rats had lower energy efficiency (P < 0.05) and tended (P = 0.10) to have less visceral fat mass. In a subsequent experiment, rats habitually fed a HF diet either continued to consume the diet or were switched to a HF+BM, low fat (LF; 7%) or LF+BM diet for 7 wk. BM was added at 0.75%. Final body weight and visceral fat mass of the two last-mentioned groups were similar to those of rats fed a LF diet for the entire duration. Rats switched to the HF+BM diet gained less weight and had less visceral fat than those fed the HF diet (P < 0.05). The addition of BM did not change apparent fat absorption. BM supplementation to the HF diet improved insulin resistance, lowered serum insulin and leptin but raised serum free fatty acid concentration (P < 0.05). This study reveals for the first time that BM reduces adiposity in rats fed a HF diet. BM appears to have multiple influences on glucose and lipid metabolism that strongly counteract the untoward effects of a high fat diet.link_to_OA_fulltex