ABSTRACT
Objective: Wild musk melon (Cucumis melo var. agrestis, CMA) is one of the edible plants form Tamil Nadu. Traditionally, this plant was used as diabetic diet (leaves of CMA with Momordica charantia leaves), but there is no scientific report on antidiabetic action of this plant material. Hence, the current research work was designed to evaluate the antihyperglycemic and antihyperlipidemic effect of hydroalcoholic extract of CMA leaves (HALEC) in streptozotocin (STZ)-nicotinamide (NIC)-induced diabetic rats. Methods: Diabetes was induced by administration of STZ (60 mg/kg, i.p.) after 15 min of NIC (120 mg/kg i.p.) administration. The diabetic rats were treated with HALEC (300 and 600 mg/kg, p.o., respectively) for 21 d. Results: After the management with HALEC, blood glucose, HbA1c levels, total cholesterol, LDL cholesterol, triglycerides levels, glycogen phosphorylase and glucose-6-phosphatase levels were significantly diminished in diabetic rats. However, haemoglobin level, HDL cholesterol, liver glycogen, total protein, hexokinase, glucose-6-phosphate dehydrogenase levels were significantly increased in HALEC treated diabetic rats. The histopathological studies of the pancreas in HALEC-treated diabetic rats showed almost normal appearance. L6 cell line study revealed the increased glucose uptake activity of HALEC. High performance thin layer chromatography (HPTLC) analysis confirms the presence of active principles such as rutin, gallic acid and quercetin in HALEC. Conclusion: The results indicated that HALEC possess significant antihyperglycemic and antihyperlipidemic activity in STZ-NIC-induced type II diabetic rats with protective effect. This research work will be useful for the isolation of active principles and development of herbal formulation in phytopharmaceuticals.
ABSTRACT
Objective:To screen the active fractions from purple sweet potatoes containing flavonoids with insulin resistance impro -ving ability.Methods:L6 cell model with insulin resistance was established .The extracting solutions with different polarity of purple sweet potato flavonoids were used to affect the model .The residual glucose concentration in insulin resistant L 6 cells was observed and compared before and after the intervention .Results:The residual glucose concentration of total flavonoids extracting solution , butanol extracting solution at middle and high dose , and chloroform extracting solution at all doses of purple sweet potato were lower than that of IR group (P<0.05).Conclusion:The total flavonoids extract, chloroform extracting solution and butanol extracting solution of purple sweet potato can improve insulin resistance in L 6 cells.
ABSTRACT
Toxoplasma gondii infection induces alteration of the host cell cycle and cell proliferation. These changes are not only seen in directly invaded host cells but also in neighboring cells. We tried to identify whether this alteration can be mediated by exosomes secreted by T. gondii-infected host cells. L6 cells, a rat myoblast cell line, and RH strain of T. gondii were selected for this study. L6 cells were infected with or without T. gondii to isolate exosomes. The cellular growth patterns were identified by cell counting with trypan blue under confocal microscopy, and cell cycle changes were investigated by flow cytometry. L6 cells infected with T. gondii showed decreased proliferation compared to uninfected L6 cells and revealed a tendency to stay at S or G2/M cell phase. The treatment of exosomes isolated from T. gondii-infected cells showed attenuation of cell proliferation and slight enhancement of S phase in L6 cells. The cell cycle alteration was not as obvious as reduction of the cell proliferation by the exosome treatment. These changes were transient and disappeared at 48 hr after the exosome treatment. Microarray analysis and web-based tools indicated that various exosomal miRNAs were crucial for the regulation of target genes related to cell proliferation. Collectively, our study demonstrated that the exosomes originating from T. gondii could change the host cell proliferation and alter the host cell cycle.