Search

We generated a rat model of sciatic nerve crush injury and characterized the effects of curcumin on sciatic nerve recovery by using behavioral experiments, hematoxylin-eosin staining, toluidine blue staining, and immunohistochemical. Proteomic analysis using tandem mass tagging was performed to determine differentially expressed proteins (DEPs), and GO and KEGG pathway analyses of overlapping DEPs was conducted, following which, qPCR, western blotting, and immunofluorescence were further performed to validate the proteins of interest. Finally, a Schwann cell injury model was used to verify the effect of curcumin on potential targets. The rat model was successfully established and curcumin improved the sciatic nerve function index of rats with sciatic nerve injury (SNI) and increased the number and diameter of myelinated axons in the sciatic nerve. In the Sham group versus the Injured group and in the Injured group versus the Curcumin group, we identified a total of 4,175 proteins, of which 953 were DEPs, and 218 were known overlapping DEPs. Ten associated pathways, such as calcium signaling pathway, biosynthesis of antibiotics, and long-term potentiation, were identified. The 218 overlapping DEPs were primarily involved in negative regulation of apoptotic process, biological processes, cytoplasm cellular component, and protein binding molecular function based on GO annotation. Curcumin promoted increased expression of ApoD and inhibited the expression of Cyba in vivo and in vitro. These results indicated that curcumin promoted sciatic nerve repair through regulation of various proteins, targets, and pathways. Cyba and ApoD may be potential targets of curcumin in the treatment of SNI.

Growing evidence has indicated that microRNAs (miRNAs) are modulators of osteoarthritis (OA) development and progression. In this study, we first evaluated the anti-apoptosis and chondroprotective effects of microRNA-675-3p (miR-675-3p) on interleukin-1β (IL-1β)-stimulated human chondrocytes. The overexpression of miR-675-3p inhibited apoptosis and cartilage matrix degradation and promoted cell proliferation in human chondrocytes. Target gene prediction and luciferase reporter assays suggested that G-protein subunit γ 5 (GNG5) may be the target gene of miR-675-3p. The overexpression of miR-675-3p inhibited IL-1β-stimulated chondrocyte apoptosis, and this effect was reversed by the overexpression of GNG5. Finally, we used bioinformatic tools and biological methods to show that the long noncoding RNA X-inactive specific transcript (lncRNA XIST) could bind to miR-675-3p, which affects the expression of GNG5 mRNA. Our findings may substantiate miR-675-3p as a new treatment for OA.

Skeletal muscle injury is accompanied by inflammation, which is common in clinical practice. To data, there is no effective method to promote skeletal muscle regeneration. Here, we develop an ROS-scavenging hydrogels loaded with MSCs (Gel@MSCs), which offer a new strategy for modulating the local inflammatory microenvironment and improve the ability of skeletal muscle repair. The therapeutic scaffold consisting of ROS-degradable hydrogel could be injected into the injured site of skeletal muscle while MSCs contribute to new myofiber formation. We found that ROS-degradable hydrogel improved the survive and of MSCs ability of MSCs. Gel@MSCs inhibited the production of inflammatory factors by promoting polarization of M2 macrophages. In addition, it promoted the expression of genes and proteins related to myogenesis in MSCs. The ROS scavenged by hydrogels further reduced the inflammatory responses. We demonstrated that regeneration of damaged muscle tissue is achieved by local treatment of Gel@MSCs, due to the activated myogenic ability, increased M2 macrophages and reduced inflammatative environment.

Peripheral nerve injury is a common disease in clinic practice. Low-dose radiation exposure can increase recovery from peripheral nerve injury, but the mechanism is unclear. The objective of this study was to explore the ways that microRNAs participate in the recovery from peripheral nerve injury in rats. To explore the function of miRNAs in this process, we performed Illumina deep sequencing to investigate miRNA expression in spinal cords after X-ray irradiation. Two miRNA libraries (0 GY and 1 GY) were constructed for Illumina sequencing. The sequencing results showed that a total of 53,342,744 raw reads for the control group −0 Gy and 48,453,367 raw reads for treated group −1 Gy were obtained. After a series of selections, a total of 804 miRNAs were identified. One hundred fifty miRNAs were differentially expressed between the treated group −1 Gy and control group −0 Gy. A total of 23,652 target genes and 48,157 target sites were predicted for the 150 differentially expressed miRNAs. GO and KEGG enrichment analyses revealed that the PI3K-Akt-signaling pathway, neuroactive ligand-receptor interaction, and the MAPK signaling pathway were enriched. We demonstrated that the novelmiRNAs-360,-301,-239, and −400 targeted Vegfa and regulated its expression after irradiation. Our study revealed that many novel miRNAs were induced by X-ray irradiation, and were involved in the recovery from peripheral nerve injuries. This study provides a framework for understanding the molecular mechanisms underlying the recovery from peripheral nerve injury following exposure to X-ray irradiation.

The long term impact of SRT (100-40 days) and recovery cleaning on membrane performance of an AnMBR treating authentic municipal wastewater in a large pilot plant was assessed. Successful operation of the pilot plant at a flux of 17 LMH was maintained for a period of 536 days during which the longest period of operation without recovery cleaning or membrane replacement was 178 days. Lower SRT (40 days) reduced the fouling propensity of the mixed liquor in terms of TSS concentration and the dewaterability indicators including colloidal COD (cCOD) concentration and capillary suction time (CST). Critical fluxes ranged from 21 to 23 LMH to 25-27 LMH for SRTs of 70 and 40 days respectively and this was consistent with the reduced concentrations of TSS and improved dewaterability under the latter conditions. Recovery cleaning was found to result in substantial reduction of resistance as indicated by both pilot plant operation and clean water flux tests. The long-term fouling rate was observed to be higher with cleaned membranes as compared to virgin membranes. The lower membrane fouling with virgin membranes suggested that accumulation of foulants, which were resistant to cleaning, caused the higher fouling rates for the cleaned membranes.

The long-term (90 days) impact of dosing FeCl3 on bioprocess performance and membrane performance in a pilot AnMBR fed with authentic sewage was evaluated. The addition of 26 mg/L of FeCl3 enhanced the performance of the AnMBR with respect to removal efficiencies of COD and BOD5, but did not have a significant influence on the removal efficiencies of TKN and TP and the methane yield. The membrane was operated at a constant flux of 17 LMH and its performance was significantly improved by dosing FeCl3. This was demonstrated by a reduction in the fouling that withstood scouring stresses to values lower than 5 kPa and negligible reversible fouling for the first 75 days. The superior membrane performance was consistent with the shift of particle size distribution to the particulate fraction and the reduced colloidal and soluble substances in the sludge, especially the soluble protein, carbohydrate, Ca and S. CLSM tests showed that the addition of FeCl3 resulted in a thicker foulant layer and the deposition of protein and carbohydrate on the membrane surface was significantly reduced. Therefore a more porous foulant layer was formed and this prevented the development of a strongly-attached cake layer and pore blocking. A recovery cleaning study indicated FeCl3 dosing enhanced the efficiency of the recovery cleaning protocol. The foulants formed with the Fe-dosed sludge had greater inorganic content, as 75% of the foulant resistance was removed by citric acid. The superior membrane performance during the operation combined with enhanced cleaning efficiency by FeCl3 dosing would significantly improve the sustainability of AnMBR in municipal wastewater treatment.

was used in this study to test the fluorescence intensity of calcium ion in osteoblasts 24 hours later. (2) We used different doses of Nimodipine (2×10 M) to block the L-type voltage dependent calcium channel of osteoblasts or used different doses of ethylenediamine tetraacetic acid (EDTA, 2×10 M, chelator of Ca) to chelate the calcium ion in the culture medium. Twenty minutes later, the experimental groups were treated with hepcidin (final concentration of 100 nM) for 1 hour. Then the flow cytometry (FCM) was used in this study to test the fluorescence intensity of calcium ions in osteoblasts. (3) The hFOB 1.19 was cultured in the culture board with 12 holes. We added D2H2O into the control group and hepcidin of different concentrations into the experimental groups. M1 group (final concentration 100 nM) and M2 group (final concentration 200 nM): 1. The ability of celI proliferation was evaluated by MTT after 24 and 48 hours. 2. Annexin V/PI staining and flow cytometry were used to detect the rate of apoptosis of osteoblast 48 hours later. 3. After 15 days continuous culture, the mineralized nodes were observed by von Kossa staining. Results: (1) The fluorescence intensity of the calcium ion in osteoblasts from the control group was 56.38±36.47 (p 0.05). There were huge deferences among the simple hepcidin group with Nimodipine, EDTA and control groups (p 0.05). 2. Hepcidin can inhibit the apoptosis of osteoblasts (p