CircRNA derived from vacuolar ATPase assembly factor (circVMA21) is a newly‐researched circRNA, which is reported to adjust the degeneration of intervertebral disc. But, function of circVMA21 in infantile pneumonia is yet to be explored. The research surveyed the role of circVMA21 in lipopolysaccharide (LPS)‐caused WI‐38 cell inflammatory injury. LPS (10 μg/ml, 12 hr) was exploited to arouse WI‐38 cell inflammatory injury. Subsequently, the mediatory impacts of microRNA (miR)‐142‐3p and circVMA21 in LPS‐evoked cell injury were detected after transfection with the inhibited or overexpressed vectors. In above processes, cell behaviors of cell viability, apoptosis, and pro‐inflammatory factors were monitored. NF‐κB and JNK pathways were elucidated to showcase the feasible molecular mechanisms. Results displayed that LPS engendered WI‐38 cell inflammatory injury was alleviated as well as activated NF‐κB and JNK pathways was interdicted by miR‐142‐3p suppression. Importantly, restrained miR‐142‐3p expression was discovered in WI‐38 cells after overexpressing circVMA21. Moreover, overexpressed circVMA21 exerted the similar functions as miR‐142‐3p suppression in LPS‐triggered WI‐38 cell injury. But, the influence was clearly reversed by miR‐142‐3p overexpression. Hindered NF‐κB and JNK pathways caused by overexpressed circVMA21 was also crippled by miR‐142‐3p overexpression. The research discolsed that circVMA21 protected WI‐38 cells to resist LPS‐triggered inflammatory injury via miR‐142‐3p‐NF‐κB/JNK axis.

Background To investigate the relationship between salt taste threshold and hypertensive nephropathy in patients with essential hypertension. Methods A cross-sectional study was conducted in 346 hypertensive patients in Daping Hospital from 2017 to 2019. Among them 94 patients were hypertensive nephropathy and 252 hypertensive patients without renal damage served as controls. The salt taste threshold of patients was measured by taking different concentrations of NaCl solution. The difference in salt taste threshold between the 2 groups of patients was compared, and the correlation between salt taste threshold and hypertensive nephropathy was analyzed. Receiver operating characteristic (ROC) curve was used to analyze the value of salt taste threshold to predict hypertensive nephropathy. Results The salt taste threshold of the hypertensive nephropathy patients was significantly higher than that in hypertensive patients without renal damage [0.075 (0.050–0.100) vs. 0.050 (0.050–0.100) mol/l, P = 0.010]. As salt taste threshold increased, the renal function decreased gradually, which was manifested by the increase of urine microalbumin to creatinine ratio, blood creatinine, blood urea nitrogen, urine N-acetyl-β-glucosaminidase, and the decrease of estimated glomerular filtration rate. Logistic regression analysis showed that after adjusting for traditional risk factors, a higher salt taste threshold was an independent risk factor for hypertensive nephropathy (odds ratio = 1.299, 95% confidence interval [CI] 1.020–1.655, P = 0.034). The area under ROC curve was 0.586 (95% CI 0.520–0.652). Conclusions Salt taste threshold correlates with biochemical indicators of renal damage, and a higher salt taste threshold is a risk factor of hypertensive nephropathy in patients with essential hypertension.

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