DPP-4 inhibitors have been shown to reverse amyloid deposition in Alzheimer's disease (AD) patients with cognitive impairment. Ocimum sanctum L. leaves reported the presence of important phytoconstituents which are reported to have DPP-4 inhibitory activity. To investigate the effects of petroleum ether extract of Ocimum sanctum L. (PEOS) in Intracerebroventricular streptozotocin (ICV-STZ) induced AD rats. ICV-STZ (3 mg/kg) was injected bilaterally into male Wistar rats, while sham animals received the artificial CSF. The ICV-STZ-induced rats were administered with three doses of PEOS (100, 200, and 400 mg/kg, p.o.) for thirty days. All experimental rats were subjected to behaviour parameters (radial arm maze task and novel object recognition test), neurochemical parameters such as GLP-1, Aβ42, and TNF-α levels, and histopathological examination (Congo red staining) of the left brain hemisphere. PEOS significantly reversed the spatial learning and memory deficit exhibited by ICV-STZ-induced rats. Furthermore, PEOS also shows promising results in retreating Aβ deposition, TNF α, and increasing GLP-1 levels. The histopathological study also showed a significant dose-dependent reduction in amyloid plaque formation and dense granule in PEOS -treated rats as compared to the ICV-STZ induced rats (Negative control). The results show that extract of Ocimum sanctum L. attenuated ICV-STZ-induced learning and memory deficits in rats and has the potential to be employed in the therapy of AD.

Inflammation, oxidative stress and altered mucosal barrier permeability are potential etiopathological or triggering factors for inflammatory bowel disease (IBD). In this study, the therapeutic potential of Mangiferin was investigated in vivo in mouse model of colitis and also attempts were made to understand mechanistic insights of Mangiferin in IBD. In present study, colitis was induced by administration of 5% DSS for 11 days, followed by 3 days of DSS free period. On day 14, animals were sacrificed and colon tissues were taken for biochemical and histological analysis. Therapeutic treatment with Mangiferin after colitis induction (i.e. day 5) ameliorated symptoms of colitis (presence of blood in stools, body weight loss and diarrhea) as evidenced by reduced DAI score, attenuated the levels of catalase (CAT), reduced glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO). It also decreased the colonic pro-inflammatory mediators tumor necrosis factor (TNF-alpha), interleukin 1 beta (IL-beta) levels, matrix metalloproteinase-9 (MMP-9) activity and histopathological score. Molecular docking of Mangiferin against TNF-alpha and MMP-9 was evaluated using GLIDE software. Mangiferin demonstrated the glide score of -8.04 kcal/mol for TNF-alpha and -9.97 kcal/mol for MMP-9, which indicated its binding potential with TNF-alpha and MMP-9. In conclusion, Mangiferin reduces colonic damage in a murine model of colitis, alleviates the oxidative and inflammatory events partly through directly influencing the activity of TNF-alpha and MMP-9 and therefore might have therapeutic usefulness in the management of inflammatory bowel disease. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

Objective: To identify incidence and determinant of new-onset of diabetes after transplant (NODAT) in Indian renal transplant recipients. Methods: In this study Indian renal transplant recipients who were not diabetic before transplant and underwent kidney transplantation between July 2004 and June 2011 were enrolled. Various data of all transplant patients including age, gender, body weight, pre transplant Hepatitis C virus (HCV), Hepatitis B virus (HBV) infection status, Human Leukocyte Antigens (HLA) mismatch, maintenance immunosuppressant drug, usage of antibodies, anti rejection treatment, patients and graft survival, post-transplant infection including HCV, HBV, Herpes and Cytomegalo virus (CMV) infection were noted down. In this study patients who had taken anti diabetic medicine beyond 1 month were considered as diabetic. Results: Total 537 renal transplant recipients were enrolled in the study. Patients age (P<0.0001), body weight (P=0.042) and HLA mismatch (P=0.015) were significantly effected on prevalence of NODAT. Other parameters like sex (P=0.862), type of donor (P=0.191), pre transplant HBV (P=0.285) and pre transplant HCV (P=0.201) were not significantly affecting development of NODAT. NODAT prevalence was not significantly affected by different Calciurine Inhibitors (CNIs) (P=0.079), antibodies (P=0.671) and by anti rejection therapy (P=0.115). Post-transplant infection was significantly higher in NODAT patients (P=0.022) and mainly among them CMV infection was prevalent (P=0.002). Other infections were found similar in patients with or without NODAT. NODAT was not significantly affecting patients survival (P=0.828) and graft survival (P=0.101). Conclusion: Age more than 45 years, body weight more than 70 kilogram, HLA mismatch, tacrolimus treatment are significantly affecting development of NODAT in Indian transplant recipients. NODAT is strongly associated with development of post-transplant infection and among them CMV infection was prevalent.

Newer potent immunosuppressive medications show marked improvements in short-term allograft function but long-term allograft survival continues to be inadequate. Non immunological factors have been increasingly identified as potentially important mediators of reduced long-term renal allograft function known as chronic allograft nephropathy. H ypertension is considered as one of this non immunological risk factor for progressive graft dysfunction. Hypertension is common after transplantation and is present in 50% to 90% of renal transplant recipients. Increasingly severe post -transplantation hypertension is associated with increasing risk of graft loss, and control of hypertension is associated with improved graft survival. Hypertension is a risk factor for both CV disease and kidney graft failure. Here we discussed about post transplant hypertension and its impact on graft function. We also discussed about causes of HT following renal transplant with special emphasis on role of immunosuppressive medication in development of hypertension. At the end we have reviewed management of post transplant HT.

In the present study, we investigated the effect of the aqueous extract of Mucuna pruriens, against cisplatin induced oxidative stress and nephrotoxicity in rats. Nephrotoxicity was induced by a single dose of cisplatin (5 mg/kg body weight i.p.). Cisplatin administration resulted in significant increases in urine volume, serum creatinine and urea and significant decrease in creatinine clearance and urinary sodium in comparison with control. Also, the renal tissue from the cisplatin treated rats showed significant decreases in the kidney glutathione content, superoxide dismutase and catalase activity and a significant increase in lipid peroxides levels. Seven days after M. pruriens extract at a dose of 200 and 400 mg/kg plus cisplatin treatments significantly decrease urea, creatinine and significantly increase creatinine clearance levels as compared to cisplatin rats in a dose dependent manner. In addition, M. pruriens prevented the rise of lipid peroxides and the reduction of superoxide dismutase, catalase and glutathione activities in a dose dependent manner. These results suggest that M. pruriens extract has protective effects against cisplatin induced oxidative stress and nephrotoxicity in rats. Key words: Mucuna pruriens, cisplatin, lipid peroxidation, free radicals.

Although coenzyme Q10 (CoQ10) is a component of the oxidative phosphorylation process in mitochondria that converts the energy in carbohydrates and fatty acids into ATP to drive cellular machinery and synthesis, its effect in type I diabetes is not clear. We have studied the effect of 4 wk of treatment with CoQ10 (10 mg/kg, ip, daily) in streptozotocin (STZ)-induced (40 mg/kg, iv in adult rats) type I diabetes rat models. Treatment with CoQ10 produced a significant decrease in elevated levels of glucose, cholesterol, triglycerides, very-low-density lipoprotein, low-density lipoprotein, and atherogenic index and increased high-density lipoprotein cholesterol levels in diabetic rats. CoQ10 treatment significantly decreased the area under the curve over 120 min for glucose in diabetic rats, without affecting serum insulin levels and the area under the curve over 120 min for insulin in diabetic rats. CoQ10 treatment also reduced lipid peroxidation and increased antioxidant parameters like superoxide dismutase, catalase, and glutathione in the liver homogenates of diabetic rats. CoQ10 also lowered the elevated blood pressure in diabetic rats. In conclusion, CoQ10 treatment significantly improved deranged carbohydrate and lipid metabolism of experimental chemically induced diabetes in rats. The mechanism of its beneficial effect appears to be its antioxidant property.

The present investigation was undertaken to study the benefical effects of Coenzyme Q10 in streptozotocin (STZ)-induced type I diabetic rats. STZ-diabetes produced a significant increase in fasting glucose levels that was associated with decrease in serum insulin levels. STZ also produced hypercholesterolemia, hypertriglyceredemia, increase in lipid peroxidation and decrease in high density lipoprotein (HDL) levels. Treatment with Coenzyme Q10 produced a significant decrease in fasting glucose levels without affecting insulin levels. Coenzyme Q10 was also found to decrease significantly AUCglucose and no significant change in AUCinsulin values in STZ-diabetic rats. Treatment with Coenzyme Q10 also caused decrease in serum cholesterol, serum triglyceride levels and an increase in HDL levels. Coenzyme Q10 treatment also reduced lipid peroxidation in diabetic rats. The elevated blood pressure in diabetic rats was also lowered. Our data suggest that Coenzyme Q10 has beneficial effects in diabetes induced complications.