RESUMEN
Background: Huntington's disease is an inherited progressive neurodegenerative disorder caused by an expansion of the polyglutamine tract leading to malformation and aggregation of the mutant huntingtin protein in the cell cytoplasm and nucleus of affected brain regions. The development of neuroprotective agents from plants has received considerable research attention. Objective: Our study aims to investigate the neuroprotective effects of luteolin and the mechanisms that underline its potential mediated protection in the mutant htt neuroblastoma cells. Methods: The mutant htt neuroblastoma cells were transfected with 160Q, and the control wild-type neuroblastoma cells were transfected with 20Q htt for 24 h and later treated with luteolin. Cell viability was determined by MTT and PI staining in both groups, while western blotting was used to evaluate caspase 3 protein expression. Aggregation formation was assessed via immunofluorescence microscopy. Also, western blotting was utilized to measure the protein expression of mutant htt aggregated and soluble protein, Nrf2 and HO-1. The impact of Nrf2 on luteolin-treated neuroblastoma cells was assessed using small interfering RNAs. Results: Our study reports that luteolin can protect cultured cells from mutant huntingtin cytotoxicity, evidenced by increased viability and decreased apoptosis. Also, luteolin reduced the accumulation of soluble and insoluble mutant huntingtin aggregates in mutant htt neuroblastoma cells transfected with 160Q compared to the control wild-type. The mutant htt aggregate reduction mediated by luteolin appeared to be independent of the Nrf2 -HO-1 antioxidant pathway. Conclusion: Luteolin presents a new potential therapeutic and protective agent for the treatment and decreasing the cytotoxicity in neurodegenerative diseases such as Huntington's disease.
RESUMEN
This study aims to investigate CAM use among CD patients from Qassim, Saudi Arabia and to compare CAM practice with different demographic and disease characteristics of the participants. A cross-sectional study was conducted among CD patients. During the three-months of data collection period, a total of 377 patients were approached and 208 patients participated in the study, giving a response rate of 55.17%. A p value of <0.05 was considered as significant. Among the study population, 94 (45.2%) patients were CAM users. Diabetes mellitus patients were the majority (48 (51.06%)) followed by hypertensive patients (34 (36.17%)). Spiritual therapies were the most common CAM followed by herbal products. Among CAM users, 41 (19.7%) patients reported disclosing CAM use to their health care providers. Among all the sociodemographic variables, gender (p = 0.029), marital status (p = 0.034) and education level (p = 0.047) were significantly associated with CAM use. In conclusion, the use of CAM among CD patients was relatively high in Qassim. Patients reported using CAM without disclosing to their health care providers which is a major health risk. It is critical to counsel CD patients regarding rational and informed CAM use in order to prevent harmful and unwanted effects.
RESUMEN
BACKGROUND: Methotrexate is an antagonist of folic acid that has been shown to be genotoxic to healthy body cells via induction of oxidative stress. Cilostazol is a phosphodiesterase III inhibitor and a potent antioxidant drug. OBJECTIVE: To evaluate the potential protective effect of cilostazol on methotrexate genotoxicity. METHODS: The genotoxic effect of methotrexate by measuring the frequency of chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs) in human cultured lymphocytes was studied. RESULTS: Methotrexate significantly increased the frequency of CAs and SCEs (p < 0.0001) as compared to control cultures. This chromosomal damage induced by methotrexate was considerably decreased by pretreatment of the cells with cilostazol (P < 0.01). Moreover, the results showed that methotrexate resulted in a notable reduction (P < 0.01) in cells kinetic parameters, the mitotic index (MI) and the proliferative index (PI). Similarly, cilostazol significantly reduced the mitotic index, which could be related to the anti-proliferative effect (P < 0.01). CONCLUSION: Methotrexate is genotoxic, and cilostazol could prevent the methotrexate-induced chromosomal damage with no modulation of methotrexate-induced cytotoxicity.
