Inflammasomes are intracellular complexes involved in the innate immunity that convert proIL-1β and proIL-18 to mature forms and initiate pyroptosis via cleaving procaspase-1. The most well-known inflammasome is NLRP3. Several studies have indicated a decisive and important role of NLRP3 inflammasome, IL-1β, IL-18, and pyroptosis in atherosclerosis. Modern hypotheses introduce atherosclerosis as an inflammatory/lipid-based disease and NLRP3 inflammasome has been considered as a link between lipid metabolism and inflammation because crystalline cholesterol and oxidized low-density lipoprotein (oxLDL) (two abundant components in atherosclerotic plaques) activate NLRP3 inflammasome. In addition, oxidative stress, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and lysosome rupture, which are implicated in inflammasome activation, have been discussed as important events in atherosclerosis. In spite of these clues, some studies have reported that NLRP3 inflammasome has no significant effect in atherogenesis. Our review reveals that some molecules such as JNK-1 and ASK-1 (upstream regulators of inflammasome activation) can reduce atherosclerosis through inducing apoptosis in macrophages. Notably, NLRP3 inflammasome can also cause apoptosis in macrophages, suggesting that NLRP3 inflammasome may mediate JNK-induced apoptosis, and the apoptotic function of NLRP3 inflammasome may be a reason for the conflicting results reported. The present review shows that the role of NLRP3 in atherogenesis can be significant. Here, the molecular pathways of NLRP3 inflammasome activation and the implications of this activation in atherosclerosis are explained.

Atherosclerosis is a progressive and multifactorial disease which occurs under the influence of various risk factors including endothelial dysfunction (ED), oxidative stress, and low-density lipoprotein (LDL) oxidation. In contract to the initial hypotheses on the usefulness of vitamin E supplementation for cardiovascular disease prevention, large outcome trials showed consumption of vitamin E has no obvious effect on cardiovascular disease and, in some cases, it may even increase the rate of mortality. This seemingly unexpected finding may be due to the opposite effects of vitamin E compounds. Vitamin E is a group of compounds which have different and even opposing effects, yet in most of the studies, the exact consumed component of vitamin E is not determined. It appears that the combined consumption of gamma-tocopherol, vitamin C, D, and tetrahydrobiopterin (BH4) may be extremely effective in both preventing atherogenesis and suppressing plaque development. In this regard, one of main issues is effect of vitamins E and D deficiency on microRNAs network in atherosclerosis. Various studies have indicated that miRNAs have key roles in atherosclerosis pathogenesis. The deficiency of vitamins E and D could provide a deregulation for miRNAs network and these events could lead to progression of atherosclerosis. Here, we highlighted a variety of mechanisms involve in the progression of atherosclerosis and effects of vitamins D and E on these mechanisms. Moreover, we summarized miRNAs involve in atherosclerosis and their regulation by vitamins E and D deficiency. J. Cell. Physiol. 232: 2968-2976, 2017. © 2016 Wiley Periodicals, Inc.

Background: Lifestyle intervention is considered first-line therapy for Nonalcoholic Fatty Liver Disease (NAFL). Objectives: Here, we aimed to compare the effect of combined Aerobic Training (AT) and Vitamin D (Vit D) supplementation on NAFLD in elderly women with Vit D deficiency. Methods: We recruited 40 women (60 -65 years) with NAFLD (second or third grade) and Vit D deficiency. Then, using simple randomization, the subjects were assigned to four groups including aerobic training (AT; 60% -75%, 20 -40 min/day, 3 days/wk running and walking), vitamin D supplementation (Vit D; 50,000 IU one day/week), aerobic training plus vitamin D supplementation (AT + Vit D), and sedentary control (C; placebo). The data were analyzed using paired t-test and one-way analysis of variance and Tukey's post hoc test with SPSS21 at a significance level of P < 0.05. Results: After eight weeks of intervention, fatty liver grade markedly reduced in the AT + Vit D, AT, and Vit D groups (60%, 38.88%, and 22% respectively). However, it increased by 17.60% in the control group. The combination of AT + Vit D significantly reduced liver enzymes, anthropometric indices, and glycemic indices and improved lipid profile. All groups demonstrated a significant inverse correlation between vitamin D and fatty liver grade. Conclusions: A sedentary lifestyle and Vit D deficiency accelerate the NAFLD probably by deteriorating hepatic risk factors. Additionally, adequate levels of plasma vitamin D are necessary to achieve the beneficial metabolic effects of aerobic training.

Epidemiologic study of dental trauma in patients presenting to the dental clinic of

The purpose of this study was to evaluate the effects of moderate-intensity resistance exercise on postexercise hypotension (PEH) in the hypertensive. The study was conducted with eighteen hypertensive elderly individuals (20-30 years). They were subjected to two experimental sessions: control session (SC) and 50% (S50%) of 1RM. For each session, subjects were evaluated pre-and postintervention. In the preintervention, the blood pressure (BP) and FVR were measured after 10 min of rest. Thereafter, they were taken to the gym to perform the exercise sessions or remained at rest in each of the equipment during the same time. I n t h e S50% group was composed of a set of ten repetitions of ten exercises, with an interval of 90 s between exercises. Subsequently, the FVR and BP measurements were again performed at 15, 30, 45, 60 and 75 min of recovery (postintervention). The PEH was greater in S50% compared with SC, with the lower value of BP being found at 75 min of recovery for the two sessions (systolic BP: 125.21 ±0.98mmHg versus 145.45 ±1.72 mmHg; diastolic BP: 83.60 ±1.67 mmHg versus 95.14 ±0.74 mmHg respectively). Moderateintensity resistance exercise was effective in promoting PEH, this phenomenon being accompanied by a reduction in FVR within the first minute of recovery in the hypertensive young.