Endurance Exercise Training Attenuates the Waterpipe Smoke Inhaling-Induced Learning and Memory Impairment in Rats: Role of Neurotrophic Factors and Apoptotic System.

INTRODUCTION: The increasing prevalence of waterpipe tobacco smoking (WTS) and its detrimental effects on memory function have been reported. This study was conducted to investigate the effect of moderate-intensity endurance exercise on the detrimental effects of WTS on learning and spatial memory in rats. AIMS AND METHODS: Animals were divided into the Control group (CTL), the exercise group (Ex) which trained for 8 weeks, the WTS group (Wp) exposed to smoke inhalation (30 minutes per day, 5 days each week, and for 8 weeks), and the group that did exercise training and received waterpipe smoke together (Ex + Wp). Thereafter, learning and spatial memory were assessed by the Morris water maze test and hippocampal molecular measurements were done. RESULTS: Waterpipe smoke significantly impaired learning and spatial memory, decreased expression of neurotrophic factors IGF-1 and BDNF (p < .01 and p < .05 vs. CTL group, respectively), increased BAX to BCL-2 ratio (p < .001 vs. CTL group) in hippocampal tissue, and increased the percent of damaged neurons in the hippocampal CA1 area (p < .05 vs. CTL group). Combination of exercise training with WTS prevented learning and spatial memory disturbances and recovered expression of neurotrophic factors IGF-1 (p < .05 vs. Wp group), decreased BAX to BCL-2 ratio (p < .001 vs. Wp group), and reduced percentage of damaged neurons (p < .05 vs. Wp group). CONCLUSIONS: Findings suggest that moderate-intensity endurance exercise training can ameliorate learning and memory impairment caused by waterpipe smoke in rats. This effect partly results from increasing the expression of neurotrophic factors BDNF and IGF-1 and correcting pro/anti-apoptotic proteins balance in the hippocampal tissue. IMPLICATIONS: The popularity of WTS especially among youth is increasing. We assessed the effect of hookah smoke with/without exercise on learning and memory. Hookah smoke leads to CA1-neural injury and impairs learning and memory in rats. A combination of exercise training with hookah smoke attenuates these complications. This positive effect of exercise is partially mediated by the balancing of brain-derived neurotrophic factor (BDNF) and Insulin-like growth factor-1 (IGF-1) and also the BAX to BCL-2 ratio, a significant predictor of cell susceptibility to apoptosis. Extrapolation of these positive findings to humans needs complementary studies.

Aquaporin 4 in Traumatic Brain Injury: From Molecular Pathways to Therapeutic Target.

Traumatic brain injury (TBI) is known as an acute degenerative pathology of the central nervous system, and has been shown to increase brain aquaporin 4 (AQP4) expression. Various molecular mechanisms affect AQP4 expression, including neuronal high mobility group box 1, forkhead box O3a, vascular endothelial growth factor, hypoxia-inducible factor-1 α (HIF-1 α) sirtuin 2, NF-κB, Malat1, nerve growth factor and Angiotensin II receptor type 1. In addition, inhibition of AQP4 with FK-506, MK-801 (indirectly by targeting N-methyl-D-aspartate receptor), inactivation of adenosine A2A receptor, levetiracetam, adjudin, progesterone, estrogen, V1aR inhibitor, hypertonic saline, erythropoietin, poloxamer 188, brilliant blue G, HIF-1alpha inhibitor, normobaric oxygen therapy, astaxanthin, epigallocatechin-3-gallate, sesamin, thaliporphine, magnesium, prebiotic fiber, resveratrol and omega-3, as well as AQP4 gene silencing lead to reduced edema upon TBI. This review summarizes current knowledge and evidence on the relationship between AQP4 and TBI, and the potential mechanisms involved.