Cigarette smoke is a complex mixture of toxic chemicals, including nicotine, carbon monoxide, and several recognized carcinogens and mutagens. Nicotine has a direct disturbing influence on steroid hormones (estrogen and progesterone), which are essential components of the female reproductive system, but the effect of nicotine on the hormone receptors is not yet clear. The aim of this study was to elucidate the effect of nicotine on the expression of estrogen receptor (ER), progesterone receptor (PR), and vascular endothelial growth factor (VEGF) in endometrial stromal cells. Expression levels of PR, ER, and VEGF in human endometrial stromal primary cells treated with nicotine (0, 10, 10, and 10μM) for 24 h were measured by quantitative real-time PCR. MTT assay demonstrated that nicotine decreased cell viability in a dose-dependent manner. Real-time PCR data showed that despite decrease in ER expression in the nicotine-treated groups compared with the control, nicotine exerted an increased inhibitory effect on PR expression compared to that on ER expression. VEGF mRNA expression in nicotine-treated endometrial stromal cells was increased. The results from this study provide novel evidence for inhibitory effects of nicotine on steroid hormones receptor expression in human primary endometrial cells. Also, our data suggest that nicotine might have angiogenesis effects on these cells.
The human multidrug resistance (MDR1) gene product P-glycoprotein is highly expressed in intestinal epithelial cells, where it constitutes a barrier against xenobiotics, bacterial toxins, drugs and other biologically active compounds, possibly carcinogens. In this study, an association of MDR1 gene polymorphism and the occurrence of colorectal cancer were evaluated. In this case-control-designed 118 unrelated colorectal cancer and 137 sex-and-ages matched healthy controls were enrolled. The C3435T MDR1 gene polymorphism was identified using the polymerase chain reaction-restriction fragment length polymorphism method. Significantly increased frequencies of the 3435T allele and the 3435TT were observed in patients with colorectal cancer compared with controls (P = 0.03; OR, 95% CI; 1.46 for 3435T allele and P = 0.003; OR, 95% CI; 2.2 for 3435TT genotype). In contrast, frequency of genotype TT was significantly higher in controls compared to colorectal cancer (P = 0.006; OR, 95% CI; 0.49 for TC genotype). In this study suggest that C3435T MDR1 polymorphism has an association with colorectal cancer. The results support that the presence of allele C results in decreased susceptibility to colorectal cancer.
Quercetin has a strengthening effect on the differentiation of rat bone marrow mesenchymal stem cells into β-cells and increases insulin secretion from the differentiated β-cells in vitro.
Background
Vitamin D (Vit.D) has an important role in protecting COVID‐19 patients. This study investigated the changes in vitamin D receptor (VDR) expression and interleukin 6 levels in patients with COVID‐19.
Materials and methods
120 hospitalized patients and 120 healthy people participated in this study, both group adjusted by sex and age. Vit.D was measured with HPLC, the expression of VDR gene was done with Real‐time PCR, and IL‐6 was measured with ELISA assay.
Results
Our findings showed no significant difference in the case of Vit.D (25‐OH‐D3) between the two studied groups, interestingly the expression of VDR was statistically lower in the patients with COVID‐19, p‐value = 0.003. VDR expression was lower in the patient with diabetes, hypertension and cardiovascular disease, significantly, p‐value = 0.002. The level of IL‐6 was statistically higher in the COVID‐19 group, p‐value = 0.003.
Conclusion
Alongside the important role of 25‐OH‐D3 in COVID‐19 patients, the quality and quantity of the VDR expression and its role in the level of IL‐6 are the promising risk factors in the future. Further studies are needed to determine the factors increasing the expression level of VDR, especially in the patients with diabetes, hypertension and cardiovascular disease.
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