The effect of TEMPOL pretreatment on postoperative cognitive function, inflammatory response, and oxidative stress in aged rats under sevoflurane anesthesia.

INTRODUCTION: The heterocyclic compound 4-hydroxy-(2,2,6,6-Tetramethylpiperidin-1-yl)oxyl (TEMPOL) has a protective effect on neurological function in brain tissues damaged by ischemia and hypoxia. This study explored the effects of TEMPOL pretreatment on postoperative cognitive function in aged rats under sevoflurane anesthesia, focusing on inflammatory response and oxidative stress. METHODS: Sixty male rats were divided into normal control (C), sevoflurane anesthesia (S), TEMPOL pretreatment (T), and sevoflurane anesthesia + TEMPOL pretreatment (ST) groups (15 per group). Groups T and ST rats received continuous intraperitoneal TEMPOL (100 mg/kg) for 3 days, while groups C and S rats were injected with 0.9% saline. After pretreatment, groups S and ST received 3% sevoflurane anesthesia. RESULTS: Rats in group S exhibited a longer swimming distance, longer escape latency, lower frequency of platform crossing, and shorter dwell time in the targeted quadrant than those in groups C and T. Rats in group ST exhibited a shorter swimming distance, shorter escape latency, higher frequency of platform crossing, and longer dwell time in the targeted quadrant than those in group S. The expressions of interleukin-6, tumor necrosis factor-α, inducible nitric oxide synthase, and Ym1/2 messenger ribonucleic acid were higher in groups S and ST rats than in groups C and T rats and lower in group ST rats than in group S rat (p < .05). Superoxide dismutase (SOD), total antioxidant capacity (T-AOC), and glutathione peroxidase (GSH-Px) were lower, while malondialdehyde (MDA) was higher in groups S and ST rats than in groups C and T rats (p < .05). Group ST showed higher SOD, T-AOC, and GSH-Px, and lower MDA than group S (p < .05). CONCLUSIONS: TEMPOL pretreatment attenuated postoperative cognitive impairment induced by sevoflurane anesthesia in aged rats. This may be attributed to the downregulation of NR2B-CREB-BDNF pathway, reducing the inflammatory response and oxidative stress damage in hippocampal tissue.

lncRNA FEZF1­AS1 contributes to cell proliferation, migration and invasion by sponging miR­4443 in hepatocellular carcinoma.

As one of the most common and aggressive cancer types, hepatocellular carcinoma (HCC) leads to a large number of fatalities every year. However, the pathogenesis of HCC remains largely unknown. In the present study, it was identified that FEZF1­AS1 was significantly upregulated in HCC cell lines and tissues, as determined by reverse transcription­quantitative polymerase chain reaction. Additionally, it was observed that higher expression of FEZF1­AS1 in patients with HCC indicated poorer prognosis. Furthermore, it was identified that knockdown of FEZF1­AS1 markedly inhibited the proliferation, colony formation, migration and invasion of Hep3B and Huh7 cells, as determined by Cell Counting Kit­8, colony formation and Transwell assays. In terms of mechanism, it was observed that FEZF1­AS1 acted as a sponge for microRNA (miR)­4443. The results of a luciferase reporter assay revealed that overexpression of miR­4443 significantly inhibited the luciferase activity in Hep3B and Huh7 cells. Additionally, miR­4443 overexpression markedly inhibited the expression of FEZF1­AS1, and vice versa. It was additionally identified that miR­4443 was downregulated in HCC tissues. There was an inverse correlation between the expression of miR­4443 and FEZF1­AS1 in HCC tissues. Furthermore, through functional experiments, it was identified that knockdown of FEZF1­AS1 significantly inhibited the proliferation, migration and invasion of HCC cells, whereas inhibition of miR­4443 reversed these effects. Collectively, the present results demonstrated that FEZF1­AS1 acts as an oncogene by acting as a sponge for miR­4443.