Activity

A hypertrophic scar (HS) is a severe fibrotic skin disease that causes disfigurement and deformity. It occurs after deep cutaneous injury and presents a major clinical challenge. The present study aimed to evaluate the effects of umbilical cord-derived mesenchymal stem cells (UCMSCs) on hypertrophic scar fibroblasts (HSFs), one of the main effector cells for HS formation, in a co-culture system and to investigate the potential underlying molecular mechanism. Cultured HSFs were divided into control and co-culture groups. The proliferation ability of HSFs was evaluated using cell counting kit-8 and the percentage of Ki67-positive fibroblasts was assessed by immunofluorescence. The apoptosis of HSFs was determined using a TUNEL assay and by assessing the expression of capase-3 via western blotting. A scratch wound healing assay was employed to examine the migration of HSFs. The expression levels of HS-associated genes (collagen type Iα 2 chain, collagen type IIIα 1 chain and actin α 2 smooth muscle) and proteinsCMSCs may exert an anti-fibrotic action on HSFs in co-culture through inhibition of the TGF β1/Smad3 pathway, which suggests a potential use for UCMSCs in HS therapy.Gastric cancer (GC) is a common cancer worldwide and its precise mechanism is largely unknown. The aim of the present study was to evaluate the expression levels of NOD-like receptor X1 (NLRX1), tumor necrosis factor receptor-associated factor 6 (TRAF6) and NF-κB in GC and normal gastric tissue samples to determine the association with the clinicopathological features of GC. GC and adjacent normal gastric tissues from 60 patients with GC were analyzed using immunohistochemistry and western blotting analysis. In addition, the association between NLRX1, TRAF6 and NF-κB expression levels were investigated by Spearman’s correlation analysis. The results revealed that NLRX1 protein expression levels were downregulated in the GC tissues compared with the normal gastric tissues (P less then 0.05). Conversely, TRAF6 and NF-κB protein expression levels were upregulated in the GC tissues compared with the normal gastric tissues (P less then 0.05). A significant difference was identified between GC patients with high and low expression levels of each protein in the tumor size, vascular invasion, neural invasion, lymph node metastasis, differentiation, gross stage and clinical stage. In addition, a negative correlation was observed between NLRX1 and TRAF6, and NLRX1 and NF-κB expression levels, while a positive correlation was observed between TRAF6 and NF-κB expression levels. In conclusion, NLRX1 expression levels were discovered to be downregulated in GC tissues. The expression levels of NLRX1, TRAF6 and NF-κB were also significantly associated with the clinicopathological characteristics of GC, and the aforementioned results indicated that NLRX1 may be a biomarker in assessing GC.The aim of the present study was to investigate the effect of dexpanthenol on nerve healing following neurorrhaphy in lacerated peripheral nerves. A total of 30 mature Sprague Dawley rats were used. Surgical sciatic nerve dissection and repair was performed on an experimental group of 20 rats. The remaining 10 rats were designated as the control group. The experimental group was divided into 2 subgroups. The surgery + saline group (SSLE; n=10) was given 1 ml/kg 0.9% sodium chloride saline intraperitoneally. The surgery + dexpanthenol group (SDPL; n=10) rats were given 500 mg/kg/day dexpanthenol intraperitoneally. Histological evaluation of the sciatic nerve tissue revealed that the fibrosis score was significantly lower in the SDPL group than in the SSLE group (P less then 0.001). Electrophysiological evaluation of compound muscle action potential (CMAP) indicated that the CMAP level in the SDPL group was significantly higher than that of the SSLE group (P less then 0.001), and the CMAP latency period was lower in the SDPL group compared with the SSLE group (P less then 0.001). In addition, the SDPL group malondialdehyde level was significantly lower than that of the SSLE group (P less then 0.001). Functional evaluation with an inclined plane test revealed a significant difference between the SSLE (39.6±5.5˚) and SDPL (79.1±6.93˚) groups (P less then 0.001). Dexpanthenol was observed to have a positive effect on nerve tissue repaired with neurorrhaphy in a rat sciatic model of laceration-type injuries similar to those frequently encountered in the clinic.The chaperone protein heat shock protein 60 (HSP60) is considered a tumor promoter in several types of primary human tumors, where it orchestrates a broad range of survival programs. Curcumin (CCM) is well-established to exhibit several anticancer properties with an excellent safety profile. Our previous study showed that CCM suppresses extracellular HSP60 expression, which is typically released by activated microglia, and acts as an inflammatory factor by binding to Toll-like receptor 4 (TLR-4) on the cell membrane. click here The present study assessed whether CCM exerted its anti-neuroglioma effects on U87 cells via inhibition of HSP60/TLR-4 signaling, similar to that in microglia. The results demonstrated that CCM significantly inhibited the viability and invasive capacity of neuroglioma U87 cells as evidenced by a Cell Counting Kit-8 assay. Western blotting and ELISA results showed that CCM decreased the expression of HSP60 and its transcriptional factor, heat shock factor 1, and reduced HSP60 release. Accordingly, TLR-4, as the target of HSP60, and its downstream signaling proteins myeloid differentiation primary response 88 (MYD88), NF-κB, inducible nitric oxide synthase and cytokines IL-1β and IL-6 were downregulated by CCM. The expression levels of apoptotic factors associated with NF-κB activation, including TNF-α and caspase-3 were increased in U87 cells by CCM treatment, while p53 expression, a tumor suppressor, was shown to be decreased. Based on the results of the present study, CCM may exert its anti-tumor effects in U87 cells by inhibiting the HSP60/TLR-4/MYD88/NF-κB pathway and inducing tumor cell apoptosis. Thus, CCM may be used as a potential therapy for the clinical treatment of neuroglioma.