Objectives The changes in testosterone level and its correlation with the endothelial nitric oxide systems balance in patients with coronary artery disease (CAD) remains uncertain. Therefore, in our study, we aimed to evaluate the levels of testosterone, endothelin-1 (ET-1), nitric oxide (NO), and endothelial NOS (eNOS) in CAD patients, and control group to find the relationship between these parameters and disease severity. Methods Forty-four patients as CAD group with significant (≥50%) stenosis confirmed by angiography was included in the study, and 40 healthy men were included as the control group. According to the number of vessels obstruction, CAD severity was determined. The serum indicated parameters were assessed to discriminate between patients and controls. Results It was found that testosterone levels in the CDA group were significantly lower than those of the control group (p<0.05). In addition, the level of ET-1 in the CAD group was higher than that in the control group, but levels of NO and eNOS in observation were significantly lower than those in the control group (p<0.05). The correlation analysis revealed that testosterone was passivity correlated with serum NO levels (r=0.550, p=0.001). Conclusions The current study reports that serum levels of testosterone are closely related to endothelial NO levels and might be of relevance to the pathogenesis of endothelial dysfunction and disease severity in CAD patients.
Background: This current study evaluated the underlying mechanisms of LF against the in ammatory miRNAs, HMGB1 expression and TLR4-MyD88-NF-кB pathway in LPS-activated murine RAW264.7 cells. Methods: MTT assay was used to assess cell viability and the cell culture levels of the cytokines (TNF-α, IL-6) were evaluated by Enzyme-linked immunosorbent assay (ELISA). The expression of miRNAs was quanti ed by using qPCR and expression of HMGB1, TLR4, MyD88, and phosphorylated NF-κB (P-p65) were determined with Western blot and qPCR, respectively.Results: The results indicated that LF downregulates IL-6 and TNF-α expression. LF exhibited the degradation of P-p65 and reduced the production of HMGB1, TLR4, and MyD88 in LPS-induced in ammatory response. Importantly, in parallel with the suppression of cytokines and HMGB1-TLR4-MyD88-NF-кB pathway, LF could induce a decrease in in ammatory selected miRNAs, miR-155 and miR-146a expression.Conclusions: Altogether, these ndings provide LF as a prominent anti-in ammatory agent could modulate HMGB1, microRNA-155, microRNA-146 and TLR4/MyD88/NF-кB pathway.
Objective: This current study evaluated the underlying mechanisms of LF against the inflammatory microRNAs (miRNAs), HMGB1 expression and TLR4-MyD88-NF-кB pathway in LPS-activated murine RAW264.7 cells. Methods: MTT assay was used to assess cell metabolism and the cell culture levels of the cytokines (TNF-α, IL-6) were evaluated by Enzyme-linked immunosorbent assay (ELISA). The expression of miRNAs was quantified by using qPCR and expression of HMGB1, TLR4, MyD88, and phosphorylated NF-κB (P-p65) were determined with Western blot and qPCR, respectively. Results: The results indicated that LF downregulates IL-6 and TNF-α expression. LF exhibited the degradation of P-p65 and reduced the production of HMGB1, TLR4, and MyD88 in LPS-induced inflammatory response. Importantly, in parallel with the suppression of cytokines and HMGB1-TLR4-MyD88-NF-кB pathway, LF could induce a decrease in inflammatory selected miRNAs, mmu-mir-155 and mmu-mir-146a expression. Conclusions: Altogether, these findings provide LF as a prominent anti-inflammatory agent could modulate HMGB1, mmu-mir-155, mmu-mir-146a and TLR4/MyD88/NF-кB pathway.
Objective: Amnion membrane (AM) has been popular for the treatment of inflammatory disorders due to its cell repairing properties. This current study aims to find the underlying mechanisms of amnion membrane proteins (AMPs) against the pro-inflammatory miRNA, miR-155, miR-146, and antiapoptotic microRNA, miR-21, in LPS-treated H9c2 cells. Methods: Cell viability and apoptosis were determined by MTT assay and annexin V/PI staining. The production of the cytokines, TNF-a and IL-6 were evaluated by using qPCR and Enzyme-linked immunosorbent assay (ELISA), respectively. In addition, the expression of miRNAs was quantified by qPCR, and also the protein level of TLR4 and NF-kb was determined with western blotting. Results: We found that AMPs ameliorated LPS-induced reduction of cell viability and augment apoptosis in H9c2 cells. AMPs efficiently inhibited cytokine expression (IL-6 and TNF-a) and activity of TLR4/ NF-jB pathway in LPS-treated H9c2 cells. Correspondingly, in parallel with the suppression of proinflammatory cytokines and apoptosis, AMPs mitigated pro-inflammatory miRNA, miR-155 expression, while, the expression of miR-155 was found to be increased in LPS-treated H9c2 cells. Also, AMPs activated miR-146 expression in H9c2 cells under LPS treatment. Additionally, the elevated expression of miR-21 provoked by LPS was further enhanced by AMPs. Conclusions: In conclusion, AMPs could alleviate LPS-induced cardiomyocytes cells injury via up-regulation of miR-21, miR-146, and suppression of TLR4/NF-jB pathway, which plays a key role in the down-regulation of LPS-mediated miR-155 and inflammatory cytokine expression.
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