Retrospective comparison of voglibose or acarbose as an add-on therapy to sulfonylureas in Western Indian patients with uncontrolled overweight/obese type 2 diabetes.

AIM: The study was aimed to investigate the effect of voglibose or acarbose as an add-on treatment in overweight/obese type 2 diabetes (T2DM) patients who are uncontrolled with metformin and sulfonylureas (SUs) in Western part of India. PARTICIPANTS AND METHODS: A retrospective study included 77 participants (BMI≥25kg/m(2); HbA1c level>8% and<9.5%) with overweight/obese T2DM. These participants were treated with either voglibose or acarbose. Glycemic parameters (fasting blood glucose and glycated hemoglobin [HbA1c]), bodyweight, BMI and lipid parameters were evaluated at baseline, 3-month, 6-month and 9-month of treatment. Adverse events were also captured at respective time points. RESULTS: Voglibose showed significant reduction in HbA1c and bodyweight with short duration of treatment (6 months; P<0.05 and 9 months; P<0.01) whereas acarbose showed significant reduction with longer duration of treatment (9 months; P<0.05) when compared with baseline. Moreover, both treatment groups were reported with reduction in BMI. Further, significant improvement in lipid parameters except LDL and HDL were observed in both treatment groups when compared with baseline. None of participant was discontinued due to side effects of the treatment. In addition, the frequency of hypoglycemia was decreased in both treatment groups. CONCLUSION: Voglibose or acarbose as an add-on treatment with metformin and sulfonylureas in uncontrolled obese/overweight T2DM provides desired glycemic control, reduces bodyweight and improves lipid parameters with good tolerability profile.

Alteration in the radiosensitivity of HeLa cells by dichloromethane extract of guduchi (Tinospora cordifolia).

Exposure of HeLa cells to TCE (dichloromethane extract of Tinospora cordifolia) for 4 hours before exposure to 2-Gy γ-radiation caused a significant decrease in the cell viability (approximately 50%). The surviving fraction (SF) was reduced to 0.52 after 4 hours of TCE treatment; thereafter, clonogenecity of HeLa cells declined negligibly with treatment duration up to 6 hours posttreatment. Exposure of HeLa cells to different doses of γ-radiation resulted in a dose-dependent decline in the viability of HeLa cells, whereas treatment of HeLa cells with various doses of TCE further decreased the cell viability depending not only on the irradiation dose but also on the concentration of TCE. Treatment of HeLa cells with various doses of TCE caused a significant decline in cell viability after exposure to 1 to 4 Gy γ-radiation. The increase in TCE concentration before irradiation caused a concentration-dependent reduction in the SF, and a lowest SF was observed for 4 µg/mL TCE for all exposure doses. HeLa cells treated with TCE showed an increase in lactate dehydrogenase and decrease in glutathioneS-transferase activity at all postirradiation times. Lipid peroxidation increased up to 4 hours postirradiation and declined gradually up to 12 hours postirradiation.

Evaluation of the radioprotective effect of Ageratum conyzoides Linn. extract in mice exposed to different doses of gamma radiation.

The effect of various doses (0, 25, 50, 75, 100, 125, 150, 300, 600 and 900 mg kg(-1)) of the alcoholic extract of the plant Ageratum conyzoides Linn. (ACE), on the alteration of radiation-induced mortality in mice exposed to 10 Gy of gamma radiation was studied. The acute toxicity studies showed that the drug was non-toxic up to a dose of 3000 mg kg(-1), the highest dose that could be tested for acute toxicity. Administration of ACE resulted in a dose-dependent decline in radiation-induced mortality up to a dose of 75 mg kg(-1), the dose at which the highest number of survivors (70.83%) was observed. Thereafter, the number of survivors declined with increasing doses of ACE and a nadir was reached at 900 mg kg(-1) ACE. Since the number of survivors was highest for 75 mg kg(-1) ACE, this was considered the optimum dose for radioprotection and used in further studies in which mice were treated with 75 mg kg(-1) ACE before exposure to 6, 7, 8, 9, 10 and 11 Gy of gamma radiation. The treatment of mice with 75 mg kg(-1) ACE reduced the severity of symptoms of radiation sickness and mortality at all exposure doses, and a significant increase in survival was observed compared with the non-treated irradiated group. The ACE treatment effectively protected mice against the gastrointestinal as well as bone marrow related death, as revealed by the increased number of survivors at all irradiation doses. The dose reduction factor was found to be 1.3. To understand the mechanism of action, various doses of ACE were evaluated for their in-vitro scavenging action on 1,1-diphenyl-2-picrylhydrazyl (DPPH), a chemically stable free radical. ACE was found to scavenge DPPH radicals in a concentration-dependent manner, indicating that the radioprotection afforded by ACE may be in part due to the scavenging of reactive oxygen species induced by ionizing radiation.

Alteration in the glutathione, glutathione peroxidase, superoxide dismutase and lipid peroxidation by ascorbic acid in the skin of mice exposed to fractionated gamma radiation.

BACKGROUND: In spite of the immense therapeutic gains produced by the fractionated irradiation (IR) regimen, radiation burden on the skin increases significantly. Protection of skin might enable use of higher radiation doses for better therapeutic gains. Ascorbic acid (AA), an essential ingredient of the human diet, is known to be a free radical scavenger and radioprotective agent. This study was undertaken to evaluate the effect of ascorbic acid on the radiation-induced changes in the status of glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and lipid peroxidation (LPx) in the skin of mice exposed to 10, 16 and 20 Gy of fractionated gamma radiation. METHODS: One group of the animals was administered daily with double distilled water (DDW), while the other group received 250 mg/kg b. wt. of ascorbic acid once daily, consecutively for 5, 8 or 10 days, before hemibody (below rib cage) exposure to 2 Gy/day of gamma-rays. Skin biopsies from both the groups were collected for the biochemical estimations. RESULTS: The irradiation of animals resulted in a dose-dependent decline in the activities of superoxide dismutase, glutathione peroxidase and glutathione contents. Ascorbic acid pretreatment resulted in a significant increase in the activities of both the enzymes and glutathione in the irradiated mouse skin. Normal concentrations of glutathione could not be restored even by day 6 post-irradiation. Conversely, lipid peroxidation increased in a dose-dependent manner in both the groups reaching a peak concentration by 3 h post-irradiation, while the ascorbic acid pretreatment inhibited the radiation-induced increase in lipid peroxidation. CONCLUSIONS: The ascorbic acid treatment arrested the decline in the activities of superoxide dismutase and glutathione peroxidase, glutathione contents and inhibited the radiation-induced lipid peroxidation in the skin of mice exposed to different doses of fractionated gamma radiation.

Evaluation of the effect of ascorbic acid treatment on wound healing in mice exposed to different doses of fractionated gamma radiation.

Alteration of the radiation-induced changes in wound contraction, collagen synthesis and wound histology by ascorbic acid was studied in mice exposed to 10, 16 and 20 Gy of fractionated (2 Gy/fraction) gamma radiation. The animals were given double-distilled water or ascorbic acid daily before exposure to 2 Gy/day of fractionated irradiation. A full-thickness skin wound was created on the dorsum of the irradiated mice, and the progression of wound contraction and collagen synthesis were examined and histological evaluations were carried out at various times after wounding. Irradiation caused a dose-dependent delay in wound contraction, and pretreatment with ascorbic acid resulted in a significant increase in wound contraction. The greatest increase in wound contraction was observed 6 and 9 days after wounding in both groups. Pretreatment with ascorbic acid augmented the synthesis of collagen significantly as revealed by an increase in hydroxyproline content. The collagen deposition and fibroblast and vasculature densities declined in a dose-dependent manner in groups receiving radiation alone as indicated by histological evaluation. Pretreatment with ascorbic acid ameliorated the observed effect significantly. These studies demonstrate that pretreatment with ascorbic acid resulted in a significant reduction of radiation-induced delay in wound healing as shown by earlier wound closure and increased collagen content and fibroblast and vascular densities.