Dose dependence and therapeutic window for the neuroprotective effects of curcumin in thromboembolic model of rat

Dohare, Preeti; Garg, Puja; Jain, Vikas; Nath, Chandishwar; Ray, Madhur

doi:10.1016/j.bbr.2008.06.012

Cited by 81 publications

(56 citation statements)

References 54 publications

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“…Evidence in experimental stroke models suggests that a single dose within 30 min to 1 h of focal cerebral ischemia protects against peroxynitrite-mediated BBB disruption (32, 57). Delayed treatment within 4 h of ischemia has also been observed to reduce infarct size and improve neurological outcomes after stroke (14). In the present study, we did not anticipate further reductions in infarct volume in diabetic animals because the lesion size was already very small in untreated animals.…”

Section: Discussionmentioning

confidence: 41%

Targets of vascular protection in acute ischemic stroke differ in type 2 diabetes

Kelly-Cobbs

Prakash

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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transformation is an important complication of acute ischemic stroke, particularly in diabetic patients receiving thrombolytic treatment with tissue plasminogen activator, the only approved drug for the treatment of acute ischemic stroke. The objective of the present study was to determine the effects of acute manipulation of potential targets for vascular protection [i.e., NF-B, peroxynitrite, and matrix metalloproteinases (MMPs)] on vascular injury and functional outcome in a diabetic model of cerebral ischemia. Ischemia was induced by middle cerebral artery occlusion in control and type 2 diabetic Goto-Kakizaki rats. Treatment groups received a single dose of the peroxynitrite decomposition catalyst 5,10,15,20-tetrakis(4-sulfonatophenyl)prophyrinato iron (III), the nonspecific NF-B inhibitor curcumin, or the broadspectrum MMP inhibitor minocycline at reperfusion. Poststroke infarct volume, edema, hemorrhage, neurological deficits, and MMP-9 activity were evaluated. All acute treatments reduced MMP-9 and hemorrhagic transformation in diabetic groups. In addition, acute curcumin and minocycline therapy reduced edema in these animals. Improved neurological function was observed in varying degrees with treatment, as indicated by beam-walk performance, modified Bederson scores, and grip strength; however, infarct size was similar to untreated diabetic animals. In control animals, all treatments reduced MMP-9 activity, yet bleeding was not improved. Neuroprotection was only conferred by curcumin and minocycline. Uncovering the underlying mechanisms contributing to the success of acute therapy in diabetes will advance tailored stroke therapies. minocycline; curcumin; 5,10,15,20-tetrakis(4-sulfonatophenyl)prophyrinato iron (III); nuclear factor-B; vascular protection WITHIN THE NEXT DECADE, the number of individuals living with diabetes is expected to rise dramatically (8). By 2030, the estimated global prevalence of the disease will exceed 437 million (53), and the vascular damage sustained during the course of the disease will increase the likelihood that these affected individuals will develop micro-and macrovascular complications, including acute ischemic stroke (AIS) (41). Historically, individuals 65 yr and older are disproportionately affected, but for the first time ever, there is an alarming increase in the number of Americans who are diagnosed at a younger age and face a prolonged course of diabetes (46). This trend poses a serious problem because recent findings suggest that the risk of AIS increases 3% with each year of diabetes and triples after 10 yr (5). In addition, diabetes complicates ischemic injury, leading to increased morbidity and poor functional recovery (7), but how diabetes worsens ischemic stroke is not fully delineated. Understanding these subtleties is essential in identifying targets for neurovascular protection and for developing therapeutic strategies tailored to this burgeoning at-risk population.In a series of studies, we showed that there is extensive cerebrovascular remodeling and ...

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Section: Discussionmentioning

confidence: 41%

Targets of vascular protection in acute ischemic stroke differ in type 2 diabetes

Kelly-Cobbs

Prakash

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…(Figure 3b) direct reacts with ONOO -in vitro [141] and protects neuronal cells by decreasing oxidative damage and suppressing glial activation [141][142][143] . Curcumin (Figure 3a) was reported to attenuate the ONOO --induced BBB breakdown and ameliorate the brain damage during cerebral ischemia-reperfusion injury [144] . Green tea catechins ( Figure 3c) protected the penumbra from ischemic reperfusion injury, which is thought be a result of decreases in iNOS expression and ONOO -level [145] .…”

Section: Uric Acidmentioning

confidence: 99%

Targeting reactive nitrogen species: a promising therapeutic strategy for cerebral ischemia-reperfusion injury

Chen

et al. 2012

Acta Pharmacol Sin

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Ischemic stroke accounts for nearly 80% of stroke cases. Recanalization with thrombolysis is a currently crucial therapeutic strategy for re-building blood supply, but the thrombolytic therapy often companies with cerebral ischemia-reperfusion injury, which are mediated by free radicals. As an important component of free radicals, reactive nitrogen species (RNS), including nitric oxide (NO) and peroxynitrite (ONOO -), play important roles in the process of cerebral ischemia-reperfusion injury. Ischemia-reperfusion results in the production of nitric oxide (NO) and peroxynitrite (ONOO -) in ischemic brain, which trigger numerous molecular cascades and lead to disruption of the blood brain barrier and exacerbate brain damage. There are few therapeutic strategies available for saving ischemic brains and preventing the subsequent brain damage. Recent evidence suggests that RNS could be a therapeutic target for the treatment of cerebral ischemia-reperfusion injury. Herein, we reviewed the recent progress regarding the roles of RNS in the process of cerebral ischemic-reperfusion injury and discussed the potentials of drug development that target NO and ONOO -to treat ischemic stroke. We conclude that modulation for RNS level could be an important therapeutic strategy for preventing cerebral ischemiareperfusion injury.

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“…Tumeric contains curcumin, demethoxycurcumin and bisdemethoxycurcumin which is potential as antioxidant and neuroprotective agent. [14][15][16] Its highly lipophylic character would increase curcumin disposition in the brain. 17 In vitro and in vivo studies showed that curcumin could prevent neurodegenerative process caused by oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Tumeric Rhizome (Curcuma Longa L) on Radial Arm Maze and Passive Avoidance Test in Trimetiline-Induced Rat Models

Yuliani

Setiani

2017

JKKI

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Backround:Oxidative stress can cause death of hippocampal cells associated to the deficit of learning and memory function. Turmeric rhizome contains curcuminoid which has antioxidant activity that can prevent oxidative stress, thus it was expected to prevent the deficit of learning and memory function on trimethyltin (TMT)-induced rat models. Objectve: This study aimed to determine the effect of turmeric rhizome extract on cognitive learning and memory fuction which was tested using radial arm maze and passive avoidance tests on Wistar rats injected with TMT. Methods: A total of 30 Wistar rats, male, 8-12 weeks of age were divided into 6 groups. The first (normal) group was given CMC-Na, the second (TMT) group was given CMC-Na, the third-the fifth groups were given turmeric rhizome extract (TRE) orally in the dosage of 120mg/kgBW (TRE120), 240 mg/kgBW (TRE240) and 480 mg/kgBW (TRE480), respectivelly. The sixth (P500) group was given piracetam in the dosage of 500 mg/kgBW. Treatments were given for 8 days orally. At day-9th, excluding the first group, all rats were injected with 12 mg/kgBW TMT solution intraperitoneally. One day after TMT injection, the cognitive learning and memory function was measured using radial maze and passive avoidance tests. The datas of cognitve function tests were analyzed statistically by ANOVA test followed by LSD test at significance level 0.05. Results:The results of radial maze and passive avoidance tests showed that the TRE240 group was not statistically significant different with TMT group(p>0.05). However there were significant difference between TRE120 and TMT groups, as well as between TRE480 and TMT groups (p<0.05). The administration of 480 mg/kgBW of TRE showed that its cognitive function was not significantly different with the administration of Piracetam (p>0.05). Conclusion: It can be concluded that the administration of 480 mg/kgBW of TRE can improve cognitive learning and memory function of Wistar rats injected by TMT. Latar Belakang: Stres oksidatif dapat menyebabkanterjadinya kematian sel hippocampus yang dapat berakibat terhadap penurunan fungsi kognitif belajar dan mengingat. Rimpang kunyit (Curcuma longa L) mengandung kurkuminoid yang memiliki aktifitas antioksidan sehingga dapat mencegah stres oksidatif dan diharapkan dapat mencegah penurunan kemampuan belajar dan mengingat pada tikus yang diinduksi zat neurotoksik trimetiltin (TMT).

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Dose dependence and therapeutic window for the neuroprotective effects of curcumin in thromboembolic model of rat

Cited by 81 publications

References 54 publications

Targets of vascular protection in acute ischemic stroke differ in type 2 diabetes

Targets of vascular protection in acute ischemic stroke differ in type 2 diabetes

Targeting reactive nitrogen species: a promising therapeutic strategy for cerebral ischemia-reperfusion injury

The Effect of Tumeric Rhizome (Curcuma Longa L) on Radial Arm Maze and Passive Avoidance Test in Trimetiline-Induced Rat Models

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