Rabbit Anti-Human ACR Polyclonal Antibody

Acrylamide (ACR) is a known neurotoxicant which crosses the blood-brain barrier, passes the placenta and has been detected in breast milk. Hence, early-life exposure to ACR could lead to developmental neurotoxicity. The aim of this study was to elucidate if non-cytotoxic concentrations of ACR alter neuronal differentiation by studying gene expression of markers significant for neurodevelopment in the human neuroblastoma SH-SY5Y cell model. Firstly, by using RNASeq we identified two relevant pathways that are activated during 9 days of retinoic acid (RA) induced differentiation i.e. RA receptor (RAR) activation and the cAMP response element-binding protein (CREB) signalling pathways. Next, by qPCR we showed that 1 and 70 mu M ACR after 9 days exposure alter the expression of 13 out of 36 genes in the RAR activation pathway and 18 out of 47 in the CREB signalling pathway. Furthermore, the expression of established neuronal markers i.e. BDNF, STXBP2, STX3, TGFB1 and CHAT were down-regulated. Decreased protein expression of BDNF and altered ratio of phosphorylated CREB to total CREB were confirmed by western blot. Our results reveal that micromolar concentrations of ACR sustain proliferation, decrease neurite outgrowth and interfere with signalling pathways involved in neuronal differentiation in the SH-SY5Y cell model.

Renal fibrosis is a major pathological event in the development of diabetic nephropathy (DN). Baicalin is a flavonoid glycoside that possesses multiple pharmacological properties including anti-fibrotic activity. In the present study, the effects of baicalin on renal fibrosis along with related molecular basis were investigated in streptozotocin (STZ)-induced DN mouse model and high glucose (HG)-treated HK-2 human proximal tubule epithelial cell model. Renal injury was evaluated through blood urea nitrogen (BUN) and serum creatinine (Scr) levels and urine albumin creatine ratio (ACR). Renal fibrosis was assessed by type IV collagen (COLIV) and fibronectin (FN) protein expression and histopathologic analysis via Masson trichrome staining. Protein levels of COLIV, FN, NF-kappa B inhibitor alpha (I kappa B alpha), phosphorylated I kappa B alpha (p-I kappa B alpha), p65, phosphorylated p65 (p-p65), and toll-like receptor 4 (TLR4) were measured by western blot assay. MicroRNA-124 (miR-124) and TLR4 mRNA levels were detected by RT-qPCR assay. The interaction of miR-124 and TLR4 was examined by bioinformatics analysis, luciferase reporter assay, and RIP assay. Baicalin or miR-124 attenuated renal injury and fibrosis in STZ-induced DN mice. Baicalin inhibited the increase of COLIV and FN expression induced by HG through upregulating miR-124 in HK-2 cells. TLR4 was a target of miR-124. MiR-124 inhibited TLR4/NF-kappa B pathway activation and the inactivation of the NF-kappa B pathway hindered COLIV and FN expression in HG-stimulated HK-2 cells. Baicalin prevented renal fibrosis by increasing miR-124 and inactivating downstream TLR4/NF-kappa B pathway in DN, hinting the pivotal values of baicalin and miR-124 in the management of DN and renal fibrosis.