Kit (Phospho-Tyr721) ELISA Kit

Background Androgenetic alopecia (AGA) is the most common cause of hair loss affecting both men and women. There are many conflicting results about the relationship between AGA and metabolic syndrome, (MetS) and the pathogenesis of the metabolic disorders in AGA patients is not completely elucidated. Aims Evaluation of the prevalence of MetS and the possible role of RANTES in pathogenesis of the MS among AGA patients. Methods A total of 160 subjects were enrolled in this work; included 100 patients clinically diagnosed with AGA and 60 apparently healthy control subjects. They were evaluated for MS components according to National Cholesterol Education Program (NCEP) adult treatment panel 3 (ATP3) and measurement of serum RANTES level using ELISA kits. Results Metabolic syndrome was present in 30.0% of AGA patients and in 10.0% of the control group (P = .038), Studied AGA patients showed significantly higher serum RANTES when compared to control group (P value < .001). Moreover, serum RANTES levels were significantly positively correlated with BMI, FBG, TC, and LDL-c levels in AGA patients with MetS. Conclusion Metabolic syndrome components were prevalent among AGA patients. Serum RANTES level was significantly higher in all AGA patients and specifically in those with MS as it was significantly positively correlated with some MetS components which reflects its possible role in pathogenesis of MetS in AGA patients.

Atherosclerosis is a chronic cardiovascular disease and contributes to pathogenesis of most myocardial infarction and ischemic stroke. Additionally, N-methyl-d-aspartate (NMDA) receptor plays a crucial role in myocardial infarction and ischemic strokes. The aim of our study was to investigate the underlying mechanisms of memantine (MEM), the blocker of NMDA receptors, in the development of atherosclerosis. In our study, human umbilical vascular endothelial cells (HUVECs) were stimulated with low-density lipoprotein (ox-LDL) to establish an atherosclerotic cell model. Cell Counting Kit-8 (CCK-8) assay and TUNEL staining were performed to detect the cell activity and apoptosis of HUVECs, respectively. The levels of inflammatory cytokines and malondialdehyde and the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and caspase-1 were quantified with commercial assay kits. Finally, qRT-PCR assay and western blot analysis were carried out to determine the mRNA and protein expressions of inflammation-related genes in HUVECs. The results of the present study suggested that ox-LDL stimulation induced decreased viability of HUVECs, excessive inflammation, and oxidative stress, while these effects were counteracted by MEM treatment. Interestingly, MEM triggered the activation of BDNF/TrkB signaling pathway in HUVECs, and K252a, the inhibitor of the BDNF/TrkB pathway, abolished the suppressive effect of MEM on ox-LDL-induced inflammation, oxidative stress, and apoptosis in HUVECs. Overall, MEM attenuated ox-LDL-induced inflammation, oxidative stress, and apoptosis via activation of BDNF/TrkB signaling pathway in HUVECs, indicating that MEM may be defined as a novel and effective agent for atherosclerosis treatment.