Recombinant protein Schistosoma japonicum-derived molecule attenuates dextran sulfate sodium-induced colitis by inhibiting miRNA-217-5p to alleviate apoptosis.

BACKGROUND: Inflammatory bowel disease (IBD) affects millions of people worldwide and has emerged as a growing problem in industrialized nations. The lack of therapeutic targets has limited the treatment of IBD. Studies found that parasitic nematode infections can ameliorate clinical and experimental colitis. Our previous study found that rSj16, a 16-kDa secreted protein of Schistosoma japonicum produced by Escherichia coli, has protective effects on dextran sulfate sodium (DSS)-induced colitis in mice. Apoptosis is an important factor in the pathogenesis of colitis. However, it is not clear whether the effect of rSj16 on colitis is related to apoptosis. AIM: To investigate whether the protective effects of rSj16 on colitis is related to apoptosis and its mechanism. METHODS: In-vivo , colitis was induced by DSS. The severity of colitis was assessed. WB was used to detect the changes of apoptosis-related genes in colon tissues. Q-PCR was used to detect the changes of miRNA-217-5p and HNF1B. In-vitro , WB was used to detect the changes of apoptosis-related genes in intestinal epithelial cells. TUNNEL staining and flow cytometry were used to detect cell apoptosis. RESULTS: rSj16 attenuates clinical activity in DSS-induced colitis mice. TUNNEL staining and WB results showed that apoptosis was increased in colon tissue after treatment with DSS, and the apoptosis of colon tissue was significantly reduced after treatment with rSj16. Compared with normal mice, the expression of miR-217-5p was increased in colon tissue of DSS-induced colitis mice. In addition, the miR-217-5p target gene hnf1b was decreased after administration of DSS. After treatment with rSj16, the expression of miR-217-5p was decreased and the expression of HNF1B was increased compared with the DSS-treated group. When Etoposide was used in combination with miR-217-5p mimic on MODE-K cells, the expression of cleaved-Caspase-3 and Bax was increased, and Bcl-2 was decreased compared with only Etoposide treatment, the expression of HNF1B was significantly reduced, suggesting that miR-217-5p acts as a pro-apoptotic in colon epithelial cells and down-regulates the target gene hnf1b. After rSj16 administration in MODE-K cells, miR-217-5p expression was significantly decreased, HNF1B expression was increased, and apoptosis was reduced. CONCLUSION: The protective effects of rSj16 on colitis is related to apoptosis and miRNA-217-5p may be a further target for therapeutic intervention against IBD.

Biohydrogen production from waste bread in a continuous stirred tank reactor: A techno-economic analysis.

Biohydrogen production from waste bread in a continuous stirred tank reactor (CSTR) was techno-economically assessed. The treating capacity of the H2-producing plant was assumed to be 2 ton waste bread per day with lifetime of 10years. Aspen Plus was used to simulate the mass and energy balance of the plant. The total capital investment (TCI), total annual production cost (TAPC) and annual revenue of the plant were USD931020, USD299746/year and USD639920/year, respectively. The unit hydrogen production cost was USD1.34/m3 H2 (or USD14.89/kg H2). The payback period and net present value (NPV) of the plant were 4.8years and USD1266654, respectively. Hydrogen price and operators cost were the most important variables on the NPV. It was concluded that biohydrogen production from waste bread in the CSTR was feasible for practical application.