RESUMO
Background and purpose: Cisplatin-induced nephrotoxicity (CIN) remains the most prevailing unfavorable influence and may affect its clinical usage. This study sought to explore the possible impacts of curcumin on preventing CIN in human subjects. Clinical design: The investigation was a placebo-controlled, double-blinded, randomized clinical trial conducted on 82 patients receiving nano-curcumin (80 mg twice daily for five days) or an identical placebo with standard nephroprotective modalities against CIN. Data was gathered on patients' demographics, blood, urinary nitrogen, creatinine (Cr) levels, urinary electrolytes, and urine neutrophil gelatinase-associated lipocalin (NGAL) levels in treatment and placebo groups, 24 h and five days after initiating the administration of cisplatin. Findings/Results: Both investigation groups were alike considering the demographic characteristics and clinical baseline data. Curcumin administration led to a significant improvement in blood-urine nitrogen (BUN). BUN, Cr, glomerular filtration rate (GFR), and the ratio of NGAL-to-Cr considerably altered during the follow-up periods. However, the further alterations in other indices, including urinary sodium, potassium, magnesium, NGAL values, and potassium-to-Cr ratio were not statistically noteworthy. The significant differences in the NGAL-to-Cr ratio between the two groups may indicate the potential protective impact of curcumin supplementation against tubular toxicity. Curcumin management was safe and well-accepted; only insignificant gastrointestinal side effects were reported. Conclusion and implications: Curcumin supplementation may have the potential to alleviate CIN and urinary electrolyte wasting in cancer patients. Future research investigating the effects of a longer duration of follow-up, a larger participant pool, and a higher dosage of curcumin are recommended.
RESUMO
Parkinson's disease (PD) is a degenerative neurodopaminergic disease in nigrostriatum pathway of human and is responsible for most of the movement disorders. Increasing evidence suggests that an inflammatory reaction accompanies the pathological processes caused by Cyclooxygenase (COX) seen in many neurodegenerative disorders, including PD and according to the recent researches chronic use of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) decreases the risk of PD in human. In the study the rat left Substantia Nigra Pars Compacta (SNc) have been destroyed using electrical lesion (1 mA; DC; 8 Sec) to induce PD model. Then aspirin (30, 60 mg kg(-1)) and celecoxib (4, 8 mg kg(-1)) have been administrated orally to parkinsonian rats. When the animals were suffered to PD Murprogo's Method evaluated the rigidity ofparkinsonian rats. Both selective COX-2 inhibitor (celecoxib) and non-selective COX-2 inhibitor (aspirin) decreased the rigidity of parkinsonian rats p<0.05 but rigidity recovery after administration the selective COX-2 inhibitor was more than non-selective COX-2 inhibitor. These findings are additional pharmacological information which has suggested the use of NSAIDs as alternative way to treat the rigidity of PD.
