Neuroprotective Effect of Curcumin in an Experimental Rat Model of Subarachnoid Hemorrhage

Kuo, Chang-Po; Lu, Chueng-He; Wen, Li-Li; Cherng, Chen‐Hwan; Wong, Chih‐Shung; Borel, Cecil O.; Ju, Da‐Tong; Chen, Chunmei; Wu, Ching-Tang

doi:10.1097/aln.0b013e31823306f0

Cited by 42 publications

(19 citation statements)

References 36 publications

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“…models. 37,38) In accordance with previous studies, our results revealed that the reduction of GSH and SOD, but the elevation of MDA by Mn treatment in BV-2 cells. Of interest, these changes were significantly reversed by curcumin pretreatment (Table 1).…”

Section: Discussionsupporting

confidence: 82%

Protective Effects of Curcumin on Manganese-Induced BV-2 Microglial Cell Death

Park

Chun

2017

Biological & Pharmaceutical Bulletin

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Curcumin, a bioactive component in tumeric, has been shown to exert antioxidant, anti-inflammatory, anticarcinogenic, hepatoprotective, and neuroprotective effects, but the effects of curcumin against manganese (Mn)-mediated neurotoxicity have not been studied. This study examined the protective effects of curcumin on Mn-induced cytotoxicity in BV-2 microglial cells. Curcumin (0.1-10 µM) dose-dependently prevented Mn (250 µM)-induced cell death. Mn-induced mitochondria-related apoptotic characteristics, such as caspase-3 and -9 activation, cytochrome c release, Bax increase, and Bcl-2 decrease, were significantly suppressed by curcumin. In addition, curcumin significantly increased intracellular glutathione (GSH) and moderately potentiated superoxide dismutase (SOD), both which were diminished by Mn treatment. Curcumin pretreatment effectively suppressed Mn-induced upregulation of malondialdehyde (MDA), total reactive oxygen species (ROS). Moreover, curcumin markedly inhibited the Mn-induced mitochondrial membrane potential (MMP) loss. Furthermore, curcumin was able to induce heme oxygenase (HO)-1 expression. Curcuminmediated inhibition of ROS, down-regulation of caspases, restoration of MMP, and recovery of cell viability were partially reversed by HO-1 inhibitor (SnPP). These results suggest the first evidence that curcumin can prevent Mn-induced microglial cell death through the induction of HO-1 and regulation of oxidative stress, mitochondrial dysfunction, and apoptotic events.

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Section: Discussionsupporting

confidence: 82%

Protective Effects of Curcumin on Manganese-Induced BV-2 Microglial Cell Death

Park

Chun

2017

Biological & Pharmaceutical Bulletin

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“…2,21,27 It has long been known that glutamate is detrimental to neurons following SAH. 9,16,34 In an in vitro study, baicalein has been demonstrated to have a protective effect against glutamate-induced neurotoxicity. 17 In the present in vivo study, we also found that brain neurons can be protected against SAH though either direct attenuation of glutamate surge or by oxidative stress inhibition.…”

Section: Discussionmentioning

confidence: 99%

“…16,34 In the sham group, the same procedure was performed, except normal saline was injected in place of blood. Mean rectal temperature was maintained at 37 ± 0.5°C with a heating pad.…”

Section: Induction Of Experimental Sah and Groupingmentioning

confidence: 99%

“…16,34 In brief, rats were anesthetized by intraperitoneal injection of sodium pentobarbital (30 mg/kg). To make the probe firm enough for implantation, a 0.0026-in Nichrome-Formvar wire (A-M Systems) was passed through the polycarbonate tubes and the cuprophan hollow fiber (the active dialysis region) and fixed inside the PE 5 tubes with epoxy glue.…”

Section: Construction and Catheterization Of The Microdialysis Probementioning

confidence: 99%

“…16,34 In brief, the hippocampus was homogenized in a 10-mM Tris buffer and a cocktail of proteinase inhibitors. Each sample was denatured at 90°C for 10 minutes in an equal volume of sodium dodecyl sulfate sample buffer and separated by electrophoresis on a 10% polyacrylamide gel.…”

Section: Western Blot Of Glt-1mentioning

confidence: 99%

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Attenuation of neurological injury with early baicalein treatment following subarachnoid hemorrhage in rats

Kuo¹,

Chen³

et al. 2013

JNS

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ObjectBaicalein has been shown to offer neuroprotection in the ischemic brain, but its effect in subarachnoid hemorrhage (SAH) is unknown. The authors used a double-hemorrhage model to study the role of early baicalein treatment in SAH.MethodsSubarachnoid hemorrhage was induced in male Wistar rats through a repeat injection of autologous blood at a 48-hour interval. Rats subjected or not subjected to SAH received a 30-mg/kg baicalein injection 3 hours after SAH and daily for 6 consecutive days, and results were compared with those obtained in vehicle-treated control rats. Mortality of the rats was recorded. Neurological outcome was assessed daily. Cerebrospinal fluid dialysates were collected and examined for glutamate concentrations. Cerebral vasospasm (CVS), brain water content, neuron variability, expression of glutamate transporter–1 (GLT-1), immunoreactivity of astrocyte, and level of malondialdehyde, activities of superoxide dismutase (SOD), and catalase in brain tissues content were determined on post-SAH Day 7.ResultsMortality rate, neuronal degeneration, brain water content, and CVS were decreased and neurological function improved in the baicalein-treated rats. Baicalein increased astrocyte activity and preserved GLT-1, which attenuated the glutamate surge after SAH. Baicalein also provided antioxidative stress by preserving activities of SOD and catalase and decreased malondialdehydelevel after SAH. The glutamate, body weight, neurological scores, and glial fibrillary acidic protein activity were significantly correlated. The CVS was correlated with neuronal degeneration, and GLT-1 was correlated with oxidative stress.ConclusionsEarly baicalein treatment attenuated CVS and limited neurological injury following SAH. These data may indicate clinical utility for baicalein as an adjunct therapy to reduce brain injury and improve patient outcomes.

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Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation

Cai

Bai

et al. 2017

Brain and Behavior

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Background and PurposeSubarachnoid hemorrhage (SAH)‐induced cerebral vasospasm and early brain injury is a fatal clinical syndrome. Cerebral vasospasm and early brain injury are associated with inflammatory response and oxidative stress. Whether curcumin, which plays important roles to regulate inflammatory cytokines and inhibit oxidative stress, inhibits SAH‐induced inflammation and oxidative stress are largely unknown.MethodsAdult male rats underwent autologous blood injection into prechiasmatic cistern to induce SAH. Curcumin (150 mg/kg) was administered at 0.5, 24 and 48 hr post‐SAH. Mortality calculation and neurological outcomes as well as morphological vasospasm of anterior cerebral artery were studied. Superoxide dismutase, lipid peroxidation, and inflammatory cytokines (MCP‐1 and TNF‐α) expression in prefrontal region were quantified. Furthermore, p65 and phosphor‐p65 were quantitatively analyzed.ResultsCurcumin remarkedly reduced mortality and ameliorated neurological deficits after SAH induction (p < .05); morphological results showed that cerebral vasospasm in curcumin‐treated group was mitigated (p < .05). SAH‐induced MCP‐1 and TNF‐α overexpression were inhibited in curcumin‐treated group (p < .05). Importantly, phosphor‐p65 was significantly inhibited after curcumin treatment (p < .05).ConclusionsCurcumin can inhibit SAH‐induced inflammatory response via restricting NF‐κB activation to alleviate cerebral vasospasm and early brain injury.

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Neuroprotective Effect of Curcumin in an Experimental Rat Model of Subarachnoid Hemorrhage

Cited by 42 publications

References 36 publications

Protective Effects of Curcumin on Manganese-Induced BV-2 Microglial Cell Death

Protective Effects of Curcumin on Manganese-Induced BV-2 Microglial Cell Death

Attenuation of neurological injury with early baicalein treatment following subarachnoid hemorrhage in rats

Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation

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