Cognitive decline prevention in offspring of Pb+2 exposed mice by maternal aerobic training and Cur/CaCO3@Cur supplementations: In vitro and in vivo studies.

Heavy metals are considered contaminants that hazardously influence the healthy life of humans and animals as they are widely used in industry. Contact of youngsters and women at ages of parturition with lead (Pb+2) is a main related concern, which passes through the placental barricade and its better absorption in the intestine leads to flaws in the fetal developfment. However, the metals threaten animal and human life, in particular throughout developmental stages. Products existing in the nature have a major contribution to innovating chemo-preventives. As a naturally available polyphenol and necessary curcuminoid, curcumin (Cur) is a derivative of the herb Curcuma longa (L.) rhizome, which globally recognized as "wonder drug of life"; however, Cur has a limited clinical use as it is poorly dissolved in water. Therefore, to enhance its clinically relevant parameters, curcumin-loaded calcium carbonate (CaCO3@Cur) was synthesized by one step coprecipitation method as a newly introduced in this research. Initially, its structure was physio chemically characterized using FT-IR, FESEM and DLS equipment and then the cytotoxicity of lead when it was pretreated with Cur/CaCO3@Cur were assessed by MTT assay. Both Cur and CaCO3@Cur diminished the toxic effects of Pb+2 while the most protective effect on the Pb+2 cytotoxicity was achieved by pre-incubation of cells with CaCO3@Cur. Besides, the morphological changes of Pb+2-treated cells that were pre-incubated with or without Cur/CaCO3@Cur were observed by normal and florescent microscopes. A non-pharmacologic method that lowers the hazard of brain damage is exercise training that is capable of both improving and alleviating memory. In the current study, the role of regular aerobic training and CaCO3@Cur was assessed in reducing the risk of brain damage induced by lead nitrate contact. To achieve the mentioned goal, pregnant Balb/C mice were assigned to five groups (six mice/group) at random: negative and positive controls, aerobic training group and Cur and CaCO3@Cur treated (50 mg/kg/b.wt) trained groups that exposed to Pb+2 (2 mg/kg) by drinking water during breeding and pregnancy. With the completion of study, offspring were subjected to the behavioral tasks that was tested by step-through ORT, DLB, MWM and YM tests. As a result, having regular aerobic training and CaCO3@Cur co-administration with lead nitrate could reverse the most defected behavioral indicators; yet, this was not visible for both sexes and it seems that gender can also be a source of different effects in the animal's body. In fact, having regular aerobic training along with CaCO3@Cur supplementation during pregnancy may be encouraging protecting potential agents towards the toxicity of Pb+2 that could be recommended in the areas with high pollution of heavy metals.

Does Endurance Training Compensate for Neurotrophin Deficiency Following Diabetic Neuropathy?

BACKGROUND: A lack of neurotrophic support is believed to contribute to the development of diabetic neuropathy. On the other hand, neurotrophins have consistently been shown to increase in the central and peripheral nervous system following exercise, but the effects of exercise intervention on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in diabetic neuropathy are not understood. OBJECTIVES: This experimental study was designed and carried out at the Tarbiat Modares university (TMU) in Tehran, Iran, to investigate the hypothesis that increased activity as endurance training can help to increase the endogenous expression of neurotrophins in diabetic rats. METHODS: This was an experimental study with 2 × 2 factorial plans performed at TMU in Iran. Sampling was accidental and 28 adult male Wistar rats in the body mass range of 326.3 ± 8.4 g comprised the sample, with each rat randomly assigned to four groups: diabetic control (DC), diabetic training (DT), healthy control (HC), and healthy training (HT). To induce diabetic neuropathy, after 12 hours of food deprivation, an intraperitoneal injection of streptozotocin (STZ) solution (45 mg/Kg) method was used. Two weeks after STZ injection, the endurance training protocol was performed for 6 weeks; 24 hours after the last training session, the rats were sacrificed. Real-time PCR was used for BDNF and NGF expression. RESULTS: The data indicate that diabetes decreases BDNF and NGF expression in sensory (92%, P = 0.01; 90%, P = 0.038, respectively) and motor (93%, P = 0.05; 60%, P = 0.029, respectively) roots. However, NGF mRNA levels in the DT group were significantly higher than in the HC group ((7.1-fold), P = 0.01; (2.2-fold), P = 0.001, respectively, for sensory and motor roots), but this was not shown for BDNF. In addition, endurance training can increase NGF expression in healthy rats ((7.4-fold), P = 0.01; (3.8-fold), P = 0.001, respectively, for sensory and motor roots). CONCLUSIONS: This study shows that BDNF and NGF expression decreases in diabetic neuropathy. However, this decrease can be reversed through endurance training. These results also indicate that endurance training may have a potential role in compensating for neurotrophin deficiency following diabetic neuropathy.