Influences of miR-708 on cerebral ischemia-reperfusion injury through targeted regulation of ADAM17.

OBJECTIVE: The purpose of this study was to explore the influences of micro ribonucleic acid (miR)-708 on cerebral ischemia-reperfusion injury by regulating a disintegrin and metalloprotease 17 (ADAM17) in a targeted manner. MATERIALS AND METHODS: The rat model of middle cerebral artery occlusion (MCAO) was established, and the differentially expressed miRNAs in the cerebral tissues of rats with ischemia-reperfusion injury were detected via sequencing. The research was performed in control group (PC12 cells received no treatment), inhibitor group (the expression of miR-708 in PC12 cells was down-regulated using miR-708 inhibitor), and interference + inhibitor group [PC12 cells were co-treated with miR-708 inhibitor and ADAM17 small interfering RNA (siRNA)]. Then, the expression of ADAM17 in cells, proliferation ability of cells, and number of apoptotic cells were detected in each group. RESULTS: A total of 225 differentially expressed miRNAs were obtained through miRNA sequencing and bioinformatics analysis, of which miR-708, miR-169, miR-26, and miR-96 were highly expressed, whereas miR-122, miR-118, and miR-177 were lowly expressed in rats in ischemia-reperfusion group. Compared with that in control group, the level of miR-708 declined significantly in inhibitor group after treatment with miR-708 inhibitor. After treatment with miR-708 inhibitor, the protein expression level of ADAM17 in inhibitor group was evidently higher than that in control group, while its protein expression level in interference + inhibitor group was significantly decreased and restored, after interference of ADAM17 siRNA with protein expression. In comparison with control group, inhibitor group had increased apoptotic cells after miR-708 inhibitor treatment (p<0.05). Besides, after interference of ADAM17 siRNA with protein expression, there were a smaller number of apoptotic cells in interference + inhibitor group (p<0.05), showing mitigated apoptosis. Moreover, the proliferation ability of cells treated with miR-708 inhibitor in inhibitor group was weaker than that in control group (p<0.05), whereas the proliferation ability of cells in interference + inhibitor group was restored to a certain degree after ADAM17 siRNA interfered with the protein expression (p<0.05). CONCLUSIONS: MiR-708 can modulate ADAM17 in a targeted manner to affect cellular proliferation and apoptosis in cerebral ischemia-reperfusion injury.

Investigation of the clinical significance of detecting PTX3 for community-acquired pneumonia.

OBJECTIVE: To evaluate the value of PTX3 in the diagnosis of community-acquired pneumonia (CAP). PATIENTS AND METHODS: We included 170 inpatients diagnosed with CAP from January 2016 to December 2018. The patients were divided into the severe pneumonia group and the mild pneumonia group according to their condition. According to the results of pathogen detection, they were divided into the bacterial infection group, the virus infection group, the mixed infection group, and the other pathogen infection group. Clinical data including C-reactive protein (CRP), procalcitonin (PCT), white blood cell count (WBC), and neutrophil-lymphocyte ratio (NLR) were collected. Blood was collected within 24 hours, 3 days, and 7 days after admission, and the serum PTX3 level was dynamically monitored. The correlation between different groups was compared, and expression differences and dynamic changes of PTX3 were analyzed. RESULTS: PTX3, PCT, and CRP in the CAP group were higher than those in the healthy control group, and the difference was statistically significant (p<0.05). Compared with the mild group, the increase of PTX3, PCT, and CRP was also different in the severe group (p<0.05). The area under the ROC curve of PTX3 was 0.726 (sensitivity 76.08%, specificity 76.92%) when the threshold value was 32.26 ng/ml. Dynamic monitoring of PTX3 showed that the PTX3 level in severe CAP patients was significantly higher than that in mild patients (p<0.05), and the PTX3 level in both groups gradually decreased with treatment time, but the level in severe CAP patients remained at a high level on the 7th day. The main pathogens in CAP were bacteria (77 cases, 45.7%), and there was no significant difference in the PTX3 level among the patients infected with different pathogenic bacteria (p=0.311). CONCLUSIONS: The serum PTX3 level, especially the dynamic monitoring results, can be used as a biomarker to reflect community acquired pneumonia, which can provide effective auxiliary diagnosis and efficacy in monitoring for clinical practice.

Knockdown of lncRNA HCP5 protects against cerebral ischemia/reperfusion injury by regulating miR-652-3p.

Previous studies have shown that lncRNAs play crucial roles in cerebral ischemia/reperfusion injury. In this study, the function and possible mechanism of lncRNA HCP5 in cerebral ischemia/reperfusion injury was investigated. An oxygen glucose deprivation (OGD) model in N2a cells was used to simulate cerebral ischemia/reperfusion injury in vitro. The functional mechanism of lncRNA HCP5 was detected using Trypan blue staining, JC-1, MTT and dual luciferase reporter assays. The expression of apoptosis-related proteins (Bcl-2 and Bax) was measured by Western blot analysis. We found that lncRNA HCP5 was upregulated in N2a cells treated with OGD/R, and knockdown of lncRNA HCP5 enhanced cell viability and reduced cell death. In addition, miR-652-3p was found to act as a sponge for lncRNA HCP5. The overexpression of miR- 652-3p can prevent cerebral ischemic reperfusion injury, however, lncRNA HCP5 attenuated the protective effect of miR-652-3p in cerebral ischemic reperfusion injury. In conclusion, upregulation of lncRNA HCP5 may exacerbate cerebral ischemic reperfusion injury by sponging miR-652-3p.

Effects of propofol or sevoflurane anesthesia on the perioperative inflammatory response, pulmonary function and cognitive function in patients receiving lung cancer resection.

OBJECTIVE: To investigate the effects of propofol and sevoflurane anesthesia on the inflammatory response, pulmonary function and cognitive function of patients undergoing lung cancer resection and their differences. PATIENTS AND METHODS: 62 patients with lung cancer who underwent pulmonary lobectomy from January 2014 to January 2016 in Jining First People's Hospital were selected and randomly divided into two groups: the propofol group (n=31) and the sevoflurane group (n=31). Patients in the propofol group were treated with intravenous injection of propofol for anesthesia maintenance, whereas those in the sevoflurane group inhaled sevoflurane for anesthesia maintenance. All patients underwent surgical resection of the lobes by the same operator. Changes in the inflammatory response and pulmonary function of patients in the perioperative period were recorded before the induced anesthesia (t1), before one-lung ventilation (t2), after sternal closure by operation (t3) and at 24 h after operation (t4), respectively; the extubation time, eye opening time and response time of two groups of patients were recorded; mini-mental state examination (MMSE) was used to evaluate the changes in cognitive function in patients and detect the concentration of S100 calcium-binding protein ß (S100ß) in serum of patients before the induced anesthesia and at 24 h after operation, respectively. RESULTS: The difference of partial pressure of alveolar-arterial oxygen (A-aDO2), respiratory index (RI) and intra-pulmonary shunt fraction (Qs/Qt) of two groups of patients at t2 and t3 were significantly higher than those at t1 (p<0.01); during t2-t3, A-aDO2, RI and Qs/Qt of patients in the propofol group were significantly lower than those of patients in the sevoflurane group (p<0.05); the levels of interleukin-6 (IL-6) and matrix metalloproteinase-9 (MMP-9) in serum of patients after the induced anesthesia in the propofol group were significantly higher than those at t1, while the level of interleukin-10 (IL-10) was lower than that at t1 (p<0.01); during t2-t4, the levels of IL-6 and MMP-9 in serum of patients in the propofol group were significantly lower than those in patients in the sevoflurane group, while the level of IL-10 was significantly higher than that in patients in the sevoflurane group (p<0.05). The postoperative extubation time, eye opening time and response time of patients in the propofol group were significantly shorter than those of patients in the sevoflurane group (p<0.05). From intraoperative period to 24 h after operation, the prevalence rate of adverse reactions in patients in the propofol group was significantly lower than that in patients in the sevoflurane group (p<0.05); MMSE scores of two groups of patients at t4 were significantly lower than those at t1, while the concentration of S100ß was significantly higher than that at t1 (p<0.01); at t4, the MMSE score of patients in the propofol group was significantly higher than that in the sevoflurane group, while the concentration of S100ß was lower than that of patients in the sevoflurane group (p<0.05). CONCLUSIONS: Compared with sevoflurane anesthesia, propofol anesthesia can significantly reduce the perioperative inflammatory response in patients receiving lung cancer resection, shorten the recovery time after operation, protect the pulmonary function of patients, improve postoperative cognitive function, and reduce the prevalence rate of intraoperative adverse reactions.