Protective effect of lyophilized recombinant human brain natriuretic peptide on renal ischemia/reperfusion injury in mice.

Brain natriuretic peptide (BNP) has a protective effect on acute injury of the heart, brain, and lung. However, its role in acute kidney injury (AKI) remains unclear. The aim of this study was to investigate the effect of lyophilized recombinant human BNP (lrh-BNP) on AKI and the underlying molecular mechanisms. An experimental model for AKI was established using an ischemia/reperfusion (I/R) procedure. Healthy adult BALB/c mice were randomized to the sham, I/R, and lrh-BNP-treated post-I/R (BNP + I/R) groups. Post-operatively, the BNP + I/R group was subcutaneously injected with lrh-BNP (0.03 µg·kg(-1)·min(-1)), whereas the other groups received saline at the same dose. Serum creatinine (Scr) and blood urea nitrogen levels were examined; tissue staining was performed to evaluate the degree of I/R injury (IRI). Ki67 positive staining of renal tubular epithelial cells was observed using immunofluorescence confocal laser scanning to assess the effect of BNP on cell proliferation after IRI. Inflammatory factor expression levels were detected to evaluate the effect of BNP on renal inflammation. Compared with the sham group, the I/R group showed increased Scr levels, severe tubular injury of the renal outer medulla, increased Kim-1 mRNA expression, an increased number of infiltrative macrophages in the renal interstitium, and increased TNF-α, IL- 1ß, IL-6, MCP-1, and HIF-1α mRNA expression. BNP delivery significantly reduced all pathological changes in the I/R group. The protective role of BNP in murine renal IRI may be associated with its inhibition of renal interstitial inflammation and hypoxia and its promotion of renal tubule repair.

Circ_0004417 inhibits the progression of prostate cancer through sponging miR-1228.

OBJECTIVE: Circular RNAs (circRNAs) have been proved to play a vital role in tumorigenesis and progression. Nevertheless, the potential mechanism of circRNAs in prostate cancer (PC) remains unclear. In the present study, we aimed to investigate the exact role of circ_0004417 in the progression of prostate cancer. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of circ_0004417 in primary PC tissues and cell lines. In vitro experiments were conducted to explore the function of circ_0004417 in PC progression, including cell counting kit-8 (CCK-8) assay, colony formation assay and transwell assay. Furthermore, the regulatory function of circ_0004417 on miRNA, p-Akt and E-cadherin was investigated to elucidate the potential mechanisms. RESULTS: Circ_0004417 was significantly down-regulated in PC tissues and cells (p<0.05). Functional experiments proved that circ_0004417 overexpression markedly inhibited the proliferation and invasion of PC cells (p<0.05). In addition, the results demonstrated that circ_0004417 served as a sponge for miR-1228 and regulated expressions of p-Akt and E-cadherin. CONCLUSIONS: Circ_0004417 inhibits the progression of prostate cancer through sponging miR-1228. All our findings suggest that circ_0004417 can be used as a potential therapeutic target for PC.