In vivo ameliorative effect of methanolic extract of Boswellia dalzielli Hutch (Mebdh) stem bark on Triton X-100 induced hyperlipidaemia

Hyperlipidemia is a major risk factor for coronary heart diseases and ischemia that leading to high rates of mortalities. Conventionally, hyperlipidemia is managed using agents that facilitate the clearance of total cholesterol (TC), triacylglycerides (TAG) and low density lipoprotein (LDL) from the body. Despite the use of these drugs, the disease still remained a global burden that affects the quality of life. The current study was done to investigate hypolipidemic properties of the methanolic extract of Boswellia dalzielli hutch (MEBDH) stem bark in rodents. The phytochemicals of the MEBDH were screened and determined qualitatively before performing acute toxicity study to determine the LD50 of the extract. Twenty five male albino rats 2-3 months old (150-210) g were distributed randomly into five groups [Group 1: normal control received 200 μL normal saline daily for 3 weeks, Group 2: hyperlipidemic control induced by a single dose of Triton X-100 (150 mg/kg body weight) subcutaneously, followed by oral administration of 200 μL normal saline daily for 3 weeks. Group 2 and 4: hyperlipidemic rats treated orally with MEBDH (200 and 400 mg/kg body weight) respectively for 21 days. Group 5: hyperlipidemic rats treated with Simvastatin (5 mg/kg body weight) daily throughout the experimental period as positive control]. Administration of the extract did not cause any mortality regardless of the dose. However, the extract caused significant (p<0.05) decrease in TC, TAG and LDL-cholesterol levels in the treated rats. The decrease observed is significantly lower than that of untreated rats. In contrast, the level of HDL increased significantly (p<0.05) after treating the rats with the MEBDH stem bark. The extract of MEBDH possessed hypolipidemic agents and could be the potential substitute hyperlipidemic agents with side effect.Keywords: Albino Rats, Atherosclerosis, Boswellia dalzielli hutch, Coronary Heart Disease, Hyperlipidemia, Triton X10

Characterization and cytotoxicity of clausenidin from Clausena excavata Burm f. and its effects on cell cycle regulation and apoptosis of liver (hepg2) and colon (ht29) cancer cell lines

Clausena excavata Burm. f. is a wild shrub from the Rutaceae family predominantly found in tropical Asia. The plant is traditionally used in the treatment of cancers; however, its mechanism of anticancer action is still unknown. Among phytochemicals present in C. excavata are alkaloids, coumarins and limonoid. Clausenidin, a pyranocoumarin isolated from C. excavata is postulated to have anticancer effects. Thus, the objective of this study is to determine the in vitro anticancer effect of clausenidin on the liver (HepG2) and colon (HT-29) cancer cell lines. The cytotoxicity and effect of clausenidin on the HepG2 and HT-29 cell cycles were determined via acridine orange/propidium iodide, reactive oxygen species (ROS), annexin V and cell cycle assays. DNA fragmentation and ultrastructural analyses, caspase-3 and -9 as well as MMP assays of the clausenidin-treated HepG2 and HT-29 ce lls were also performed to determine the mode of cell death. In addition, apoptosis-re lated genes and proteins were also analyzed using qPCR and Western blot respectively to further verify the effects of clausenidin on HepG2 and HT-29 cells. The IC50 of clausenidin in HepG2 and HT-29 cells was 7.7 and 13.8 μg/mL at 72 hours of treatment, respectively. The results reveal that clausenidin induced G0/G1 and G2/M cell cycle arrest of HepG2 cells in a dose- and time-dependent manner. Clausenidin also caused depolarization of the mitochondrial membrane that resulted in the release of cytochrome C and significant (p0.05) change in caspase-8, JNK and VEGF protein expressions. The HT-29 cells treated with clausenidin entered a G0/G1 cell cycle arrest. These cells also underwent depolarization of mitochondrial membrane resulting in cytochrome C release and subsequent increase in caspase-9 and Bax protein expressions that resulted in the activation of the intrinsic pathway of apoptosis. Clausenidin induced activation of caspase-3 that caused fragmentation of DNA and nuclei of the HT-29 cells, which are hallmarks of apoptosis. Upon treatment with clausenidin, HT-29 cells also showed increased production of ROS that is postulated to contribute to their death. The clausenidin-treated HT-29 cells like the HepG2 cells showed typical features of apoptosis although some cells underwent necrosis. In conclusion, the study showed clausenidin isolated from C. excavata induced death of the HepG2 and HT-29 cells especially via apoptosis. Thus, clausenidin has the potential to be developed as a therapeutic compound for the treatment of liver and colon cancers

LC-MS and GC-MS Profiling of Different Fractions of Ficus platyphylla Stem Bark Ethanolic Extract

The exploration of medicinal plants in traditional medicine for the treatment of diseases has been practiced for long, globally, because of its cultural acceptability, availability, and affordability. This study investigated the qualitative and quantitative estimation of phytochemicals present in Ficus platyphylla stem bark as well as determined the reducing power and antioxidant property of each fraction against DPPH and NO radicals. The study further elucidated the presence of possible compounds in different fractions (methanol, ethyl acetate, petroleum ether, and chloroform) of Ficus platyphylla stem bark (FPSB) extract using GC-MS, LC-MS, and FTIR techniques. Qualitative phytochemical analysis reveals the presence of phytochemicals: saponin, flavonoids, tannins, phenols, steroids, alkaloids, and glycoside in the ethanolic extract. The LC-MS study of methanol and ethyl acetate fractions reveals the presence of thirteen and three compounds, respectively. GC-MS analysis shows the presence of trans-13-octadecenoic acid as the main compound 38.07% and cis-vaccenic acid as the least compound (0.10%) in the petroleum ether fraction. The main compound in the chloroform fraction is 12-oleanen-3-yl acetate, (3. alpha.) with a peak area percentage of 49.25% and oleic acid been the least compound with 0.07% peak area. The FTIR analysis reveals that the fractions contain compounds with hydroxyl, aromatic, methyl, methylene, methyne, long aliphatic chain, ethers, ether-oxy, peroxides, etc. The analyzed fractions reveal compounds with potential pharmacological activity in the management of pathological conditions

Nontoxic Glucomoringin-Isothiocyanate (GMG-ITC) Rich Soluble Extract Induces Apoptosis and Inhibits Proliferation of Human Prostate Adenocarcinoma Cells (PC-3)

The incidence of prostate cancer malignancy along with other cancer types is increasing worldwide, resulting in high mortality rate due to lack of effective medications. Moringa oleifera has been used for the treatment of communicable and non-communicable ailments across tropical countries, yet, little has been documented regarding its effect on prostate cancer. We evaluated the acute toxicity and apoptosis inducing effect of glucomoringin-isothiocyanate rich soluble extracts (GMG-ITC-RSE) from M. oleifera in vivo and in vitro, respectively. Glucomoringin was isolated, identified, and characterized using fundamental analytical chemistry tools where Sprague-Dawley (SD) rats, murine fibroblast (3T3), and human prostate adenocarcinoma cells (PC-3) were used for acute toxicity and bioassays experiments. GMG-ITC-RSE did not instigate adverse toxic reactions to the animals even at high doses (2000 mg/kg body weight) and affected none of the vital organs in the rats. The extract exhibited high levels of safety in 3T3 cells, where more than 90% of the cells appeared viable when treated with the extract in a time-dependent manner even at high dose (250 µg/mL). GMG-ITC-RSE significantly triggered morphological aberrations distinctive to apoptosis observed under microscope. These findings obviously revealed the putative safety of GMG-ITC-RSE in vivo and in vitro, in addition to its anti-proliferative effect on PC-3 cells