Qiang Fu; Dong Hai Liu; Zi Xuan Li; Xiao Peng Zheng; Cynthia Mutemwa; Elvis Agbo
Volume 25, Issue 4 , 2023
Abstract
Background: Current studies have demonstrated the anti-cancer effects of paeonol in some tumors; however, its effect on gliomas remains unknown.
Objectives: This study aimed to investigate the anti-tumor effect of paeonol in human glioma tissues and cells including its effect and connection with apoptosis ...
Read More
Background: Current studies have demonstrated the anti-cancer effects of paeonol in some tumors; however, its effect on gliomas remains unknown.
Objectives: This study aimed to investigate the anti-tumor effect of paeonol in human glioma tissues and cells including its effect and connection with apoptosis and oxidative stress in gliomas.
Methods: Cell Counting Kit-8 (CCK-8) was used to detect the antiproliferative effect of paeonol in human U251 glioma cells. Transwell and colony-forming assays were employed to assess the effect of paeonol on the ability of invasion and colony formation of U251 cells. Superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, total antioxidant capacity (T-AOC), and catalase activity (CAT) were measured to evaluate the effect of paeonol on oxidative stress in U251 cells. Quantitative real-time polymerase chain reaction (RT-q) PCR and western blot were utilized to detect caspase-3 expression levels. Terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) staining detected the effect of paeonol on U251 cell apoptosis.
Results: Paeonol decreased cell viability, as well as the proliferation, invasion, and colony formation ability of U251 cells. Paeonol reduced MDA content and increased the activities of SOD, CAT, and T-AOC in U251 cells. Caspase-3 expression was lower in human glioma tissues than in normal tissues of the human brain. Paeonol promoted U251 cell apoptosis as revealed by TUNEL staining results and the significant up-regulation of caspase-3 expression in U251 cells.
Conclusion: These results indicated that paeonol has anti-tumor and pro-apoptotic effects in gliomas via oxidative stress regulation and the caspase-3 pathway. Our study, therefore, provides new ideas for the clinical treatment of gliomas.
Elvis Agbo; Dong Hai Liu; Jia Wan Liao; Roland Osei SAAHENE; Precious Barnes
Volume 23, Issue 6 , 2021
Abstract
Background: Growth hormone-releasing peptides (GHRP) have been reported to possess cardioprotective properties; nonetheless, their mechanisms of action are still not very clear.
Objectives: Some studies have suggested that modulation of endothelial nitric oxide synthase (eNOS) and the upregulation of ...
Read More
Background: Growth hormone-releasing peptides (GHRP) have been reported to possess cardioprotective properties; nonetheless, their mechanisms of action are still not very clear.
Objectives: Some studies have suggested that modulation of endothelial nitric oxide synthase (eNOS) and the upregulation of nitric oxide (NO) are cardioprotective. Therefore, the present study strived to test the hypothesis that a potent GHRP analog (hexarelin) could increase serum nitric oxide level and regulate myocardial eNOS to alleviate the development of heart failure.
Methods: Myocardial infarction-induced heart failure in rats was established by permanent coronary artery ligation. The sham group, control group, and heart failure group all received normal saline (100 µg/kg; SC BID; 30days), while the rats in the hexarelin treatment group were treated with hexarelin (100 µg/kg, SC BID, 30 days). The rats were tested for myocardial apoptosis, oxidative stress, left ventricular function, various molecular analyses, as well as pathological and structural myocardial changes.
Results: Hexarelin treatment improved contractile function and attenuated myocardial histopathological damages, oxidative stress, ?brosis, as well as apoptosis. All these were accompanied by the upregulation of myocardial eNOS and an increase in serum NO concentration.
Conclusion: As evidenced by the obtained results, the anti-cardiac failure capacity of hexarelinin in a rat model is mediated by an increase in serum nitric oxide level and the up-modulation of myocardial eNOS; therefore, they can be considered therapeutic targets against heart failure.
