No abstract

Curcumin is widely available, inexpensive spice that has been used in ancient folk medicine for millennia, especially in India. Curcumin has the pharmacological properties that slow or reverse cellular proliferation and enhance apoptosis and differentiation associated with a diverse array of molecular effects. Despite its effective anticarcinogenesis properties, curcumin's poor solubility, instability, and extensive metabolism result in poor oral bioavailability. Strategies to enhance curcumin delivery include encapsulating or incorporating curcumin in a nanoparticle or microparticle drug delivery system, synthesizing more stable curcumin analogs that resist metabolism while retaining curcumin's pharmacological properties, and adding another natural product that has bioenhancing properties to curcumin or combination of two of these strategies. This review comprehensively explores curcumin's chemistry and pharmacology followed by comparing and contrasting a vast number of strategies designed to enhance curcumin's bioavailability and its therapeutic effects. The review provides insights into which curcumin formulation strategies have the greatest promise to reach clinical application.

Background Herbal medicines long have been used in the management of diabetes mellitus (DM). Objective This study was conducted to ascertain if fenugreek compared with glibenclamide had any impacts on controlling blood glucose in patients with uncontrolled type II DM on conventional therapy. Methods A total of 12 patients with uncontrolled DM and on metformin were recruited and divided into two groups. Patients in group 1 received 2 g fenugreek per day, whereas those in group 2 received glibenclamide 5 mg once daily. The impacts of fenugreek on the glycemic control and lipid profile were measured before initiation of the regimen and then after 12 weeks. Results Only 9 of the 12 study participants completed the study. Fenugreek at 2 g/day caused an insignificant drop in fasting blood glucose (P = 0.63), but the fasting insulin level increased significantly (P = 0.04). The ratio of high- to low-density lipoprotein was significantly decreased from before to after treatment (P = 0.006). Fenugreek did not cause any notable adverse impacts on hepatic and renal functions throughout the study. Conclusion Fenugreek could be used as adjuvant therapy to anti-diabetic drugs to control blood glucose, and further studies are needed.

Testicular toxicity of methotrexate (MTX) is a clinically important adverse effect. Ginseng has been demonstrated to stimulate spermatogenesis, prevent chemotherapy-induced testicular injury and to possess antiapoptotic and antioxidant actions. Owing to its low bioavailability, ginseng was formulated to nanoform in the current study. As there is no available data about the protective effects of ginseng or ginseng nanoparticles against MTX-induced testicular toxicity, this study was initiated. Seventytwo male rats were enrolled. Rats were given either ginseng (5oo mg/kg/day), or ginseng nanoparticles (125 and 250 mg/kg/day) orally for 28 consecutive days. Rats received a single dose of MTX (20 mg/kg) intraperitoneally on day 25. Ginseng and ginseng nanoparticles pre-treatment in rats significantly alleviated the testicular histopathological effects induced by MTX. Also, they significantly restored the impaired spermatogenesis induced by MTX via significantly increasing the Johnsen's tubular biopsy score (JTBS). Ginseng and ginseng nanoparticles treatment prior to MTX administration in rats significantly ameliorated MTXinduced testicular apoptosis by significantly decreasing the percentage of caspase-3-immunostained testicular area. Ginseng and ginseng nanoparticles pretreatment caused nonsignificant increase in serum testosterone levels that were significantly decreased by MTX. The results indicate that ginseng and ginseng nanoparticles protect against MTX-induced testicular toxicity in rats, which is suggested to be through inhibition of MTX-induced testicular apoptosis. The protective effect of ginseng nanoparticles was supposed to be better than ginseng in the given doses.

Hypothesis: This study aimed to elucidate the role of glibenclamide in the prevention of diabetic nephropathy and to compare it with a reference drug captopril in rats. Materials and methods: There were two main groups of rats. Control group (I) was subdivided into four subgroups which received distilled water, vehicle of streptozotocin, glibenclamide or captopril. The streptozotocin-diabetic Group (II) was subdivided into three subgroups: untreated, glibenclamide or captopril treated. Measurement of arterial blood pressure, serum glucose and creatinine levels, 24 h urinary protein and albumin/creatinine ratio, kidney weight and its histological examination were done after 1, 2, 4, 8, 12 and 16 weeks of treatment. Results: In treated diabetic rats captopril reduced blood pressure significantly, while no significant change in the mean arterial blood pressure or blood glucose level was recorded with glibenclamide treatment. Glibenclamide and captopriltreated diabetic rats showed significant decrease in serum creatinine level, urine volume, urinary protein excretion, albumin:creatinine ratio and kidney:body weight ratio compared with the diabetic non-treated group. Histological examination of diabetic kidneys treated with either glibenclamide or captopril showed reduced glomerular hypertrophy, glomerulosclerosis, tubular degeneration and interstitial fibrosis compared with untreated diabetic rats. Conclusion: Glibenclamide attenuated some biochemical and histological changes produced by diabetic nephropathy, despite persistent hyperglycemia and hypertension.