Is Chronic Curcumin Supplementation Neuroprotective Against Ischemia for Antioxidant Activity, Neurological Deficit, or Neuronal Apoptosis in an Experimental Stroke Model?

AIM: To investigate the neuroprotective effect of chronic curcumin supplementation on the rat forebrain prior to ischemia and reperfusion. MATERIAL AND METHODS: Forebrain ischemia was induced by bilateral common carotid artery occlusion for 1/2 hour, followed by reperfusion for 72 hours. Older rats were divided into five groups: Group I received 300 mg/kg oral curcumin for 21 days before ischemia and 300 mg/kg intraperitoneal curcumin after ischemia; Group II received 300 mg/kg intraperitoneal curcumin after ischemia; Group III received 300 mg/kg oral curcumin for 21 days before ischemia; Group IV had only ischemia; Group V was the sham-operated group. The forebrain was rapidly dissected for biochemical parameter assessment and histopathological examination. RESULTS: In forebrain tissue, enzyme activities of superoxide dismutase, glutathione peroxidase, and catalase were significantly higher in Group I than Groups II or III (p < 0.05) while xanthine dehydrogenase and malondialdehyde enzyme activities and concentrations of interleukin-6 and TNF-alpha were significantly lower in Group I when compared to Groups II and III (p < 0.05). A significant reduction in neurological score was observed after 24 and 72 hours in the curcumin-treated groups compared with the ischemic group. We also found a marked reduction in apoptotic index after 72 hours in the groups receiving curcumin. Significantly more TUNEL-positive cells were observed in the ischemic group compared to those treated with curcumin. CONCLUSION: We demonstrated the neuroprotective effect of chronic curcumin supplement on biochemical parameters, neurological scores and apoptosis following ischemia and reperfusion injury in rats.

Effects of curcumin on proinflammatory cytokines and tissue injury in the early and late phases of experimental acute pancreatitis.

BACKGROUND & AIMS: Acute pancreatitis (AP) varies from mild to severe necrotizing changes with high mortality. The objective of the current study was to investigate the effects of curcumin on tissue injury and proinflammatory cytokines in the early and late phases of AP. METHODS: AP was induced by sodium taurocholate in rats (n = 140). First group was left untreated. Group II received 100 mg/kg curcumin daily starting 20 days before AP induction. The rats were allocated into 7 sub-groups (n:5) and were sacrificed at 2, 6, 12, 24, 72, 144 and 288 h following the induction of AP. Blood and pancreatic tissue samples were collected for biochemical and histopathologic evaluations and the assessment of protein and mRNA levels, as well. RESULTS: Curcumin decreased total histopathologic scores in comparison with those of the taurocholate group (P < 0.05). Curcumin increased Caspase-3 activity and decreased trypsin activity, while inhibited nuclear factor-κ (NF-κB) at all time points (P < 0.05) and moreover reduced activator protein-1 (AP-1). Curcumin decreased chemokine (except for 288 h), TNF-α (except for 2 and 24 h), IL-6 (except for 2, 6 and 288 h) and iNOS (except for 144 and 288 h) mRNA levels (P < 0.05). Curcumin serum nitric oxide (NO) (except for 144 and 288 h) levels were reduced, as well. CONCLUSIONS: In conclusion, curcumin reduced tissue injury, trypsin activation and inhibited NF-κB and AP-1. However TNF-α, IL-6 and iNOS and NO were not inhibited at all time points. Therefore no direct correlation was detected in the subgroups between tissue injury, proinflammatory cytokines and oxidative enzymes.

Pathologic alterations detected in acute pancreatitis induced by sodium taurocholate in rats and therapeutic effects of curcumin, ciprofloxacin and metronidazole combination.

BACKGROUND AND AIMS: Secondary bacterial infections and free radical injury have been known to play an important role in the pathogenesis and clinical outcome of acute pancreatitis. Despite the therapy models developed in recent years, the mortality rate is still reported to be higher than expected. The objective of this study therefore was to investigate the effectiveness of ciprofloxacin and metronidazole combination and curcumin together in the treatment of acute pancreatitis. METHODS: Acute pancreatitis was induced in rats by sodium taurocholate (n = 60). Starting 6 h after the induction of acute pancreatitis, groups I and II were injected 200 mg/kg ciprofloxacin and 500 mg/kg metronidazole intraperitoneally every 12 h for 6 days. Groups II and III received 100 mg/kg curcumin since day 20 prior to the initiation of acute pancreatitis. On day 6, animals of all groups were killed. Blood and tissue samples were taken for biochemical, pathologic and bacteriologic examination. RESULTS: No statistical difference in the treatment groups versus the non-treatment group has been detected in the pancreatic tissue on the basis of histopathological scoring results. Prevalences of bacterial translocation were significantly lower in the treatment groups (groups I-III) than in the non-treatment group (group IV) (p < 0.001, p < 0.001, p < 0.05, respectively). Serum amylase, lipase, malon dialdehyde and nitric oxide (except for nitric oxide level in group I), levels of groups I, II and III were significantly lower than those of group IV (p < 0.05). CONCLUSIONS: The administration of ciprofloxacin and metronidazole in combination and curcumin in acute pancreatitis failed to provide a preventive effect on the occurrence of tissue injury, whereas free radical injury and prevalence of bacterial translocation were reduced significantly.