Efficacy of Butylphthalide in Combination with Edaravone in the Treatment of Acute Ischemic Stroke and the Effect on Serum Inflammatory Factors.

Objective: To investigate the efficacy of butylphthalide combined with edaravone in the treatment of acute ischemic stroke and the effect on serum inflammatory factors. Methods: One hundred and sixty patients with acute ischemic stroke who attended the neurovascular intervention department of our hospital from May 2020 to June 2022 were enrolled as study subjects for prospective analysis and were equally divided into a control group and an experimental group using the random number table method, with 80 cases in each group. The control group was treated with edaravone injection, while the experimental group was treated with butylphthalide combined with edaravone. The disease was recorded to compare the efficacy, erythrocyte sedimentation rate, homocysteine, serum inflammatory factors including tumor necrosis factor-α, C-reactive protein and interleukin-6 levels, and the incidence of adverse reactions between the two groups. Results: The total effective rate of treatment in the experimental group was 90.0% (72/80), while that of the control group was 62.5% (50/80), the total effective rate of the experimental group was significantly higher than that of the control group, and the difference was statistically significant (P < 0.05). After treatment, the erythrocyte sedimentation rate, homocysteine level, and serum TNF-α, CRP, and IL-6 levels of patients in the experimental group improved compared with those before treatment, and the degree of improvement was better than that of the control group, and the difference was statistically significant (P < 0.05). After 3 months of treatment, a comparison of the incidence of adverse reactions in the two groups showed no statistically significant difference between the two groups (P > 0.05). Conclusion: The treatment of acute ischemic stroke with butylphthalide combined with edaravone has positive significance in improving blood circulation regulation and serum inflammatory factor levels and is reliable and worthy of clinical promotion.

RNF216 Alleviates Radiation-Induced Apoptosis and DNA Damage Through Regulating Ubiquitination-Mediated Degradation of p53 in Glioblastoma.

Glioblastoma (GBM) is the most common and lethal subtype of glioma, characterized by uncontrolled cancer cell proliferation, extensive infiltration, and therapeutic resistance. Ring finger protein 216 (RNF216) is a RING-type E3 ubiquitin ligase aberrantly expressed in multiple human cancers. Tumor protein 53 (p53) is a transcription factor that acts as a tumor suppressor. This study aimed to compare the RNF216 expression in GBM tissues and normal peritumoral tissues and to examine the effects of RNF216 overexpression/knockdown on tumorigenesis, radioresistance, and the p53 pathway in GBM. The results showed that RNF216 was overexpressed in GBM tissues and cell lines, and high RNF216 expression was related to a poor prognosis. RNF216 overexpression promoted GBM cell growth and inhibited apoptosis, while RNF216 knockdown impaired GBM cell growth and enhanced cell death. RNF216 was also highly expressed in recurrent GBM tissues compared with paired primary tumors. The upregulation of RNF216 not only facilitated GBM cell growth but also protected cells against X-ray irradiation-induced apoptosis and DNA damage, while RNF216 knockdown exerted opposite effects. Moreover, the implantation of GBM cells with RNF216 silencing suppressed tumorigenesis and increased radiosensitivity of mice bearing GBM xenografts. Further analysis revealed that RNF216 overexpression reduced the stability of p53 protein via ubiquitination and negatively regulated the p53 pathway, while RNF216 knockdown preserved the p53 protein. In conclusion, RNF216 effectively attenuated radiation-induced apoptosis and DNA damage in GBM via inducing ubiquitination-mediated degradation of p53. These findings suggest the potential therapeutic use of RNF216 inhibition for tumorigenesis and therapeutic resistance in GBM.