Effect of lncRNA-MIAT on kidney injury in sepsis rats via regulating miR-29a expression.

OBJECTIVE: The long non-coding ribonucleic acid (lncRNA)-myocardial infarction associated transcript (MIAT) has been demonstrated to serve as a key regulator in various physiological and pathological processes. This study aims to explore whether lncRNA-MIAT regulates the expression of micro RNA (miR)-29a to affect kidney's injury in sepsis rats. MATERIALS AND METHODS: A total of 30 healthy male Sprague-Dawley (SD) rats were randomly divided into experimental group and control group. Rats in the experimental group were injected with lipopolysaccharide (LPS) through the tail vein to prepare the model of sepsis-induced kidney injury, while those in the control group with the equal volume of normal saline. After the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) in rats were determined to ascertain successful modeling, fluorescence quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to measure the expression levels of the lncRNA-MIAT and miR-29a messenger RNAs (mRNAs) in renal tissues. The normal rat kidney epithelial (NRK-52E) cell line was cultured in vitro, and the model was established in vitro via LPS to study the influences of lncRNA-MIAT and miR-29a on the kidney injury in sepsis rats. Moreover, cell apoptosis was detected using Western blotting. RESULTS: According to the results of the rat in vivo experiment and NRK-52E cell line in vitro experiment, the model of kidney injury was established successfully, and compared with the control group, experiment group had significantly raised SCr and BUN levels (p<0.01) and a remarkably increased lincRNA-MIAT gene expression level (p<0.01), but a substantially decreased miR-29a gene expression level (p<0.01). Additionally, when the expression of lncRNA-MIAT was up-regulated, the expression of miR-29a was prominently decreased (p<0.01), but that of the cell apoptosis gene cysteine-aspartic proteases (Caspase)-8 protein was remarkably increased (p<0.01). However, the expression of Caspase-8 protein was significantly lowered (p<0.01) once the expression of miR-29a was up-regulated. CONCLUSIONS: LncRNA-MIAT may bind to miR-29a to participate in sepsis-related kidney injury.

MiR-205 influences renal injury in sepsis rats through HMGB1-PTEN signaling pathway.

OBJECTIVE: To investigate the influences of micro ribonucleic acid (miR)-205 on renal injury in sepsis rats through the high-mobility group box 1 (HMGB1)-phosphatase and tensin homolog deleted on chromosome ten (PTEN) signaling pathway. MATERIALS AND METHODS: A rat model of sepsis-induced renal injury was established by cecal ligation and perforation. The rats were randomly divided into 3 groups, namely the Sham group, the Model group, and the miR-205 group. Hematoxylin and eosin (HE) staining was applied to examine the pathological renal morphology. The enzyme-linked immunosorbent assay (ELISA) was adopted to measure the serum levels of Caspase-3 and Bcl-2-associated X protein (Bax) in rats. Cell apoptosis rate in the renal tissues was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Finally, the protein levels of phosphorylate-HMGB1 (p-HMGB1) and p-PTEN in the renal tissues were determined using the Western blotting (WB) assay. RESULTS: Compared with those in the Sham group, the pathological morphology of the renal tissues was poor in Model group. The serum levels of Caspase-3 and Bax, the apoptosis rate, and the protein levels of p-HMGB1 and p-PTEN were remarkably enhanced in the Model group compared to the Sham group. In comparison with those in Model group, the pathological changes in renal morphology, apoptosis-related indexes, and protein levels of p-HMGB1 and p-PTEN were alleviated in the miR-205 group. CONCLUSIONS: MiR-205 agonist can improve the pathological morphology in the sepsis rats with renal injury, improve renal cell apoptosis, and inhibit the protein levels of HMGB1 and PTEN in renal tissues. MiR-205 alleviates sepsis-induced renal injury through the HMGB1-PTEN signaling pathway.

Structural analysis of anti-tumor heteropolysaccharide GFPS1b from the cultured mycelia of Grifola frondosa GF9801.

A 21-kDa heteropolysaccharide, coded as GFPS1b, was obtained from the cultured mycelia of Grifola frondosa GF9801 by hot-water extraction, ethanol precipitation, and fractioned by DEAE Sepharose Fast-flow, followed by the purification with Sephadex G-100 column chromatography using an AKTA purifier. It exhibited more potent anti-proliferative activity on MCF-7 cells than other polysaccharide fractions. GFPS1b was an acidic polysaccharide with approximately 16.60% protein and 4.3% uronic acid. Gas chromatography of absolute acid hydrolysate of GFPS1b suggested that it was composed of D-glucose, D-galactose, and L-arabinose with a molar ratio of 4:2:1. Periodate oxidation, Smith degradation, partial acid hydrolyzation, methylation analysis, FT-IR, and (1)H, (13)C NMR spectroscopy analysis revealed that GFPS1b had a backbone consisting of alpha-(1-->4)-linked D-galacopyranosyl and alpha-(1-->3)-linked D-glucopyranosyl residues substituted at O-6 with glycosyl residues composed of alpha-L-arabinose-(1-->4)-alpha-D-glucose (1--> linked residues.

Optimization of the medium composition for production of mycelial biomass and exo-polymer by Grifola frondosa GF9801 using response surface methodology.

In this work, a three-level Box-Behnken factorial design was employed combining with response surface methodology (RSM) to optimize the medium composition for the production of the mycelial biomass and exo-polymer in submerged cultures by Grifola frondosa GF9801. A mathematical model was then developed to show the effect of each medium composition and their interactions on the production of mycelial biomass and exo-polymer. The model estimated that, a maximal yield of mycelial biomass (17.61 g/l) could be obtained when the concentrations of glucose, KH2PO4, peptone were set at 45.2 g/l, 2.97 g/l, 6.58 g/l, respectively; while a maximal exo-polymer yield (1.326 g/l) could be achieved when setting concentrations of glucose, KH2PO4, peptone at 58.6 g/l, 4.06 g/l and 3.79 g/l, respectively. These predicted values were also verified by validation experiments. Compared with the values obtained by other runs in the experimental design, the optimized medium resulted in a significant increase in the yields of mycelial biomass and exo-polymer. Maximum mycelial biomass yield of 22.50 g/l was achieved in a 15-l fermenter using the optimized medium.

[The influence of hypertension and antihypertensive agents on experimental IgA nephropathy (IgAN)].

In an attempt to evaluate the influence of hypertension and antihypertensive agents on IgAN, IgAN and hypertension experimental models were induced in SD rats and divided into 4 groups: (1) IgAN(n = 8); (2) IgAN+by hypertension(n = 8); (3) captopril 4mg/100gBW/d, for 42 days administered to rats as group (2) (n = 8); (4) nifedipine 300ug/100gBW/d, for 42 days administered to rats as group (2) (n = 8). Blood pressure was measured at the 12th, 14th, 16th, 18th and 20th week. Urinary protein, serum angiotensin II (AT II) and renal pathologic changes were examined at the 20th week. Our results suggest that hypertension worsens IgAN by glomerular mesangial proliferation in early stages. Though Captopril has the same therapeutic effect on hypertension as Nifedipine does, the former has been proven to have potentially beneficial effects on diminishing proteinuria as well as mesangial lesions. This is consistent with the suppression of serum ATII which favours glomerular microcirculation.