Effects of circular antisense non-coding RNA in the INK4 locus (circANRIL) on vascular endothelial injury, oxidative stress and inflammation in rats with coronary atherosclerosis were studied by establishing a rat model of coronary atherosclerosis in which circANRIL was differentially expressed. A total of 40 healthy Sprague Dawley (SD) rats were randomly divided into research group (n=32) and control group (n=8). In research group, a rat model of coronary atherosclerosis was established without special treatment. The blood calcium (Ca 2+ ) and lipid levels in the two groups were compared. After cell transfection, the rats were divided into blank group (untransfected), negative group (transfected with blank vector), circANRIL group (transfected with circANRIL overexpression plasmid) and circANRIL inhibitor group (transfected with circANRIL silencer). Then the levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in each group were compared. Western blotting was adopted to detect the expressions of phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK), p38MAPK and glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Finally, p-p38MAPK/GAPDH, p38MAPK/GAPDH and p-p38MAPK/p38MAPK were calculated. There were significant differences in the levels of serum Ca 2+ and lipid between control group and research group (P<0.05). Besides, differences in LDH, SOD, MDA, TNF-α and IL-6 in the supernatant in each group were statistically significant (P<0.05 or P<0.01). Moreover, there were statistically significant differences in the gray values of p-p38MAPK/GAPDH and p38MAPK/GAPDH and their ratio p-p38MAPK/p38MAPK in each group (P<0.05 or P<0.01). Inhibiting the expression of circANRIL in coronary heart disease cases can reduce vascular endothelial injury, oxidative stress and inflammation.
The present study explored the effects of aspirin combined with cilostazolin in the treatment of diabetic patients with thromboangiitis obliterans and the effects on the related inflammatory factors. A total of 90 diabetic patients with thromboangiitis obliterans admitted to Weifang People's Hospital from August 2015 to June 2017 were selected and divided into the control group (n=45) and the combination group (n=45). Patients in the control group were given aspirin, and those in the combination group were given aspirin combined with cilostazol. Before treatment and 6 weeks after treatment, the clinical data including ankle-brachial index (ABI), 6-min walk test (6MWT) and test data including serum inflammatory factors interleukin (IL)-8, IL-6 and matrix metalloprotease (MMP)-2 and MMP-9 of the two groups were collected for quantitative and statistical analysis. Compared with those in the control group, the ABI and 6MWT in the combination group could be effectively reduced, and the differences were statistically significant (P<0.05). At the same time, cilostazol combined with aspirin could effectively reduce the levels of serum inflammatory factors MMP-2 and MMP-9 in patients, except for nitric oxide (NO), and the differences were statistically significant (P<0.05). Compared with that before treatment, the control and the combination group can significantly improve the clinical symptoms of the patients, and aspirin combined with cilostazol can effectively improve the clinical curative effect of diabetic patients with thromboangitis obliterans and delay the progression of the disease.
Post-transcriptional regulation and RNA-binding proteins (RBPs) play vital roles in the occurrence of secondary injury after intracerebral hemorrhage (ICH). Therefore, we identified RBPs distinctively expressed after ICH by screening and determined thioredoxin1 (Txn1) as one of the most distinctive RBPs. We employed an ICH model and in vitro experiments to investigate the role of Txn1 in ICH. Firstly, we found that Txn1 was mainly expressed in microglia and neurons in the central nervous system, and its expression was significantly reduced in perihematomal tissue. Additionally, adeno-associated virus (AAV) carrying Txn1 was injected into the ICH rat model. Our results showed that overexpression of Txn1 reduced secondary injury and improved outcome in the ICH rat model. Moreover, to understand the therapeutic mechanism of Txn1 after ICH, we performed RNA immunoprecipitation combined with high-throughput sequencing. The results showed that Txn1 binds to inflammation-and apoptosis-related mRNAs and affects gene expression through RNA splicing and translation. Finally, RNA pull-down assays and in vitro experiments confirmed that Txn1 binds to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), leading to reduced inflammation and apoptosis. Our study suggests that Txn1 is a potential therapeutic target for alleviating ICH-induced brain injury.
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