Zinc Supplementation Reduces ROS Production and Prevents MDMA-Induced Apoptosis in TM3 Leydig Cells via the Inhibition of Pro-Apoptotic Proteins.

MDMA can cause serious adverse effects on vital organs such as the heart, brain, and liver. Additionally, MDMA consumption can also potentially cause various endocrine system dysfunctions. The previous study has shown that pre-treatment of zinc can reduce the cytotoxicity of MDMA on the Leydig cell line (TM3). In this study, we investigated the mechanisms involved in the treatment with MDMA on the apoptosis of TM3 cells and the effects of zinc pre-treatment on reducing the apoptotic effects of MDMA. TM3 cells were incubated with MDMA (5 mM), zinc (8 µM), and zinc (8 µM) prior to MDMA (5 mM) for 48 h. The cells were pre-treated with zinc for 24 h prior to the administration of MDMA, and the total culture time was 48h. The effect of different treatment groups in causing oxidative stress and apoptosis in TM3 cells was measured by DCF, TUNNEL, and western blot tests, respectively. Our results revealed that the number of DCF and tunnel-positive cells increases as a result of MDMA treatment. In addition, the treatment with MDMA increased the expression of pro-apoptotic proteins caspase 3, Bax, and p53. Conversely, the expression of anti-apoptotic protein Bcl-2 decreased. Zinc pre-treatment significantly decreased the expression of pro-apoptotic proteins and the number of tunnels and DCF-positive cells compared to the MDMA-only group. It is concluded that MDMA has a toxic effect and causes apoptosis on TM3 cells, and also, pre-treatment with zinc mitigates the ROS production and toxic effect of MDMA and MDMA-induced apoptosis in TM3 cells.

Evaluation of interleukin-17 receptor (IL-17RA) gene expression in PBMCs of patients with premature coronary artery disease.

OBJECTIVES: Present study has been carried out to analyze the IL-17R gene expression in PBMCs of patients with premature coronary artery disease (CAD) in comparison to normal controls. BACKGROUND: Premature CAD results in disability and lack of quality of life over the years and consequent mortality. Cardiovascular disease (CVD) has global distribution. In 2022, CAD is the leading cause of mortality in the United States and Iran. IL-17 cytokine family plays an important role in promoting inflammation and producing pro-inflammatory cytokines, chemokines, and matrix metalloproteinases. METHODS: Entirely, 60 subjects were entered into this examination. The case group consisted of 30 subjects with CAD as well as the control group which consisted of 30 healthy persons. The real-time quantitative reverse transcription PCR assay was used to find out, the relative expression (fold) level of IL-17R gene. RESULTS: Our findings indicated that, the relative expression (fold) level of IL-17R gene in the patients group showed an increased level as compared to the control group. The analysis of findingsobtained in this study showed that the patient group is significantly different from the control group regarding the IL-17R mRNA level (fold) (p = 0.035). CONCLUSION: It has been concluded that IL-17R plays an important role in the pathogenesis of CAD. It follows that superior understanding of IL-17/IL-17R signaling way will be vital for innovating novel therapeutic targets that will facilitate the designing of new drugs for the management of patients (Ref. 40).

Interleukin-17 is Not Associated with Risk of Premature Coronary Artery Disease in Iranian Turks.

Cardiovascular diseases are one of the most important causes of death globally. Results of recent studies have indicated that cytokine dysregulation was associated with premature coronary artery disease (P-CAD). The majority of cytokine gene polymorphisms influence the level of cytokine production and secretion. This study aimed to analyse IL-17 gene expression in patients with P-CAD and healty individuals in an Iranian population. This case-control study, conducted in Urmia University of Medical Sciences, compared patients with P-CAD hospitalised for risk of coronary artery stenosis, those admitted for medical cares and healthy normal controls. Thirty patients with P-CAD and 30 healthy individuals entered the study. The tested individulas were selected according to strict criteria such as clinical, echocardiogram, electrocardiogram and coronary angiography findings. Individuals with diabetes type 1 or 2 were excluded from the study. Reducing the diameter of at least one of the coronary arteries with more than 50% obstruction was selected as P-CAD. The qRT-PCR technique was used to determine the level of IL-17 gene expression in the studied groups. IL-17 gene expression was compared between the tested groups using t-test or Mann-Whitney U-test. Subjects' mean age (±SE) was 45(±5) and 44 (±4) among tested cases and related controls, respectively. The relative mRNA expression was 4.04±2.4 in patients with P-CAD and 2.75±1.3 in controls for IL-17. IL-17 gene expression was not significantly different in the tested groups (P> 0.05). IL-17 is not associated with risk of P-CAD in Iranian Turks.

10-Hydroxy-2-Decenoic Acid Prevents Ultraviolet A-Induced Expression of Lamin AÄ150 in Human Dermal Fibroblasts.

10-Hydroxy-2-decenoic acid (10-HDA) as the main component of royal jelly has pharmacological characteristics. But the influence of 10-HDA on skin photoaging and photo damage is poorly understood. In the present study, we used 10-HAD immediately after UVA exposure and tested the effects on the attenuation of LMNAÄ150 expression in cultured human dermal fibroblasts Human dermal fibroblasts (cultured cells) were exposed to UVA irradiation. The mRNA level of LMNAÄ150 was determined by Taqman Real-Time PCR Assay. Real-time PCR analysis of LMNAÄ150 transcripts indicated that the level of LMNAÄ150 transcripts was higher in the UVA exposed group than the group treated with 10-HAD after UVA exposure (>8.22-fold). The LMNAÄ150 expression is down-regulated in human dermal fibroblasts after treatment with 10-HDA. It can be concluded that treatment with 10-HDA suppresses the UVA-induced gene expression of LMNAÄ150 and protects skin from UVA-induced photoaging and photo damage.