Background and Purpose: Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance and abnormalities in insulin production. Apelin is associated with insulin resistance. According to the anti-diabetic properties of curcumin, the purpose of this study was to compare the effects of curcumin and nano-curcumin intake on insulin resistance and serum levels of fasting blood sugar (FBS), Apelin, and lipid profile (cholesterol, triglyceride, LDL, HDL and VLDL) in T2DM rats. Materials and Methods: Forty-eight male Wistar rats were divided into six groups: Control, diabetic, diabetic treated with two doses of curcumin (100 and 200 mg/kg) and diabetic treated with two doses of nano-curcumin (100 and 200 mg/kg). Induction of T2DM was performed by intraperitoneal injection of Nicotinamide (110 mg/kg) and Streptozotocin (45 mg/kg) in the fasting state. Rats received different doses of nano-curcumin and curcumin by gavage (daily) for 28 days. At the end of the intervention period, insulin resistance and serum levels of FBS, apelin and lipid profiles were measured. Results: Insulin resistance and serum levels of FBS, Apelin, cholesterol, triglycerides, LDL, and VLDL were significantly decreased in diabetic rats treated with curcumin and nanocurcumin (p<0.05) so that nano-curcumin in reducing lipid profile is more effective than curcumin (P<0.05). Serum level of HDL in nano-curcumin groups was significantly higher than diabetic and curcumin groups (p<0.05). Also, with increasing insulin resistance, serum level of apelin increased (P<0.05). Conclusion: The therapeutic effects of curcumin and nano-curcumin were effective in decreasing insulin resistance, serum levels of FBS, apelin and lipid profile. The dose of 100 mg/kg nano-curcumin was more effective in reducing lipid profile.
(2016) Beneficial effects of ellagic acid against animal models of scopolamine-and diazepam-induced cognitive impairments, Pharmaceutical Biology, 54:10, 1947-1953, DOI: 10.3109/13880209.2015 PHARMACEUTICAL BIOLOGY, 2016 VOL. 54, NO. 10, 1947-1953 http://dx.doi.org/10.3109/13880209.2015 Context In a previous study, it has been shown that ellagic acid (EA), a polyphenolic compound found in pomegranate and different berries, prevents cognitive and hippocampal long-term potentiation (LTP) impairments induced by traumatic brain injury in rats through antioxidant and anti-inflammatory mechanisms.Objective The present study was conducted to assess the potential of EA as a memory enhancer.
Materials and methodsThe elevated plus maze (EPM) and passive avoidance (PA) paradigm were used to evaluate learning and memory parameters. Three doses (10, 30 and 100 mg/kg, i.p.) of EA were administered to animals. Memory impairment was induced by scopolamine treatment (0.4 mg/kg, i.p.) and/or diazepam (1 mg/kg, i.p.). Acquisition trials were carried out 30 min after scopolamine treatment and retention trials were performed for 5 min 24 h after the acquisition trials.Results EA at doses 30 and 100 mg/kg significantly reversed the amnesia induced by scopolamine (0.4 mg/kg, i.p.) in the EPM and PA tests in mice. Also, EA at doses 30 and 100 mg/kg significantly antagonized the amnesia induced by diazepam (1 mg/kg, i.p.) in EPM test in rats. Moreover, chronic administration of EA at dose 30 mg/kg ameliorated the memory deficit induced by diazepam (1 mg/ kg, i.p.) in rats. Discussion and conclusion This study demonstrates that ellagic acid is effective in preventing scopolamine-and diazepam-induced cognitive impairments without altering the animals' locomotion. This suggests the potential of EA application as a useful memory restorative agent in the treatment of dementia seen in elderly persons.ARTICLE HISTORY
Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. In the clinic it is essential to limit the development of cognitive impairment after TBI. In this study, the effects of gallic acid (GA; 100 mg/kg, per oral, from 7 days before to 2 days after TBI induction) on neurological score, passive avoidance memory, long-term potentiation (LTP) deficits, and levels of proinflammatory cytokines including interleukin-1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) in the brain have been evaluated. Brain injury was induced following Marmarou's method. Data were analyzed by one-way and repeated measures ANOVA followed by Tukey's post-hoc test. The results indicated that memory was significantly impaired (p < 0.001) in the group treated with TBI + vehicle, together with deterioration of the hippocampal LTP and increased brain tissue levels of IL-1β, IL-6, and TNF-α. GA treatment significantly improved memory and LTP in the TBI rats. The brain tissue levels of IL-1β, IL-6, and TNF-α were significantly reduced (p < 0.001) in the group treated with GA. The results suggest that GA has neuroprotective properties against TBI-induced behavioral, electrophysiological, and inflammatory disorders, probably via the decrease of cerebral proinflammatory cytokines.
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