Efficacy of Neuroprotection from Curcumin through Heat Shock Protein 70 Induction in Traumatic Brain Injury – Rat Model (original) (raw)
Related papers
International Journal of PharmTech Research, 2017
TBI (traumatic brain injury) results in significant disability due to cognitive deficits mainly in attention, learning and memory and higher-order executive functions. In this study we examined the effect of Curcumin on cognitive dysfunction through increase ACH and decrease caspase 3 expression in hippocampus and cortex. Twenty five anaesthetized Wistar rats were subjected to TBI using Shohami weight-drop model. The ACH and caspase 3 activity was determined using immunohistochemistry in brain tissue slices after 5 days treatment of Curcumin at 3 different doses 50 mg/kg, 100 mg/kg, 200 mg/kg and examined cognitive function using MWM. Increase expression of ACH was observed in hippocampus and cortex of brain after administration of curcumin in TBI, also was observed decrease expression of caspase 3 and improvement of cognitive dysfunction. In addition to observation above we found that increase expression of ACH no significant difference between treatment group, while decrease expression of caspase 3 was significant with high dose, and leading to good outcome of cognitive dysfunction. From our result we suggest that after TBI administration of curcumin may improve cognitive dysfunction through mechanism involving increasing of expression of ACH and decreasing of expression of caspase 3 and therefore decreasing apoptosis.
Effect of Combination Treatment of Candesartan and Curcumin on Traumatic Brain Injury in Mice
2016
Traumatic brain injury (TBI) is a severe condition and a major cause of death and disability, particularly in young adults. Traumatic brain injury invokes a complex inflammatory, oxidative and apoptotic responses. The present experimental study was designed to assess the effect of combination treatment of curcumin and candesartan on TBI in mice. Mice were classified into six groups (Sham, TBI and TBI post-treated with vehicle, curcumin, candesartan or combination of curcumin + candesartan for 7 days), n=12 each. Mice were anesthetized and then placed under a weight-drop device.The animals were killed by cervical dislocation, brains were rapidly isolated and homogenized. Traumatic brain injury group showed significant increment in MDA, TNF-Alpha, caspase-3 as compared to sham group and these effects were significantly ameliorated by curcumin, candesartan or their combination treatment. Also total antioxidant capacity (TAC) decreased markedly in the TBI group and increased significant...
Background and Aim: Traumatic brain injury (TBI) is one of the critical causes of death in trauma patients. In this study, the effect of nanocurcumin on the outcome of severe TBI was investigated for the first time in humans. Methods and Materials/Patients: This randomized, double-blind, and paralleled controlled study included 128 patients aged from 18 to 70 years with severe brain trauma. Patients were randomly assigned to control group (standard care treatment+placebo) and intervention group (standard care treatment+oral nanocurcumin). Changes in the level of consciousness, cerebral edema, kidney function, liver enzymes, sodium and potassium electrolytes, and brain function were followed up and compared until 6 months after discharge. Results: The Mean±SD in the intervention (14.44±31.86 years) and control patients (14.86±33.34 years) had no significant difference (P=0.543). Both groups were similar in terms of gender (P=0.669). The average level of consciousness in the intervention group increased by about 3 units (P=0.004) and more than 2 units (P=0.002) at discharge compared with the control group. By comparing the optimal performance of patients in the first (P=0.389) trimester and second (P=0.309) trimester after discharge, no significant difference was observed between the intervention and control groups. The amount of brain edema caused by severe brain trauma on the seventh day of treatment in the intervention group was lower than that in the control group (P=0.038). Conclusion: Administrating oral nanocurcumin supplement in patients with severe brain trauma along with their routine treatment is effective in improving brain edema and their level of consciousness without causing coagulation, and liver and kidney complications. These findings are not only statistically significant but also clinically vital.
Journal of …, 2011
Object. Intracerebral hemorrhage (ICH) is associated with significant morbidity and mortality. Acute hematoma enlargement is an important predictor of neurological injury and poor clinical prognosis; but neurosurgical clot evacuation may not be feasible in all patients and treatment options remain largely supportive. Thus, novel therapeutic approaches to promote hematoma resolution are needed. In the present study, the authors investigated whether the curry spice curcumin limited neurovascular injury following ICH in mice.
Journal of Neurochemistry, 2010
Traumatic brain injury is a devastating neurological injury associated with significant morbidity and mortality. Medical therapies to limit cerebral edema, a cause of increased intracranial hypertension and poor clinical outcome, are largely ineffective, emphasizing the need for novel therapeutic approaches. In the present study, pre-treatment with curcumin (75, 150 mg/kg) or 30 minute post-treatment with 300 mg/kg significantly reduced brain water content and improved neurological outcome following a moderate controlled cortical impact in mice. The protective effect of curcumin was associated with a significant attenuation in the acute pericontusional expression of interleukin-1β, a pro-inflammatory cytokine, after injury. Curcumin also reversed the induction of aquaporin-4, an astrocytic water channel implicated in the development of cellular edema following head trauma. Notably, curcumin blocked IL-1β-induced aquaporin-4 expression in cultured astrocytes, an effect mediated, at least in part, by reduced activation of the p50 and p65 subunits of NFκB. Consistent with this notion, curcumin preferentially attenuated phosphorylated p65 immunoreactivity in pericontusional astrocytes and decreased the expression of glial fibrillary acidic protein, a reactive astrocyte marker. As a whole, these data suggest clinically-achievable concentrations of curcumin reduce glial activation and cerebral edema following neurotrauma, a finding which warrants further investigation.
Neuroprotective Effects of Curcumin Against Transient Global Ischemia are Dose and Area Dependent
Archives of Neuroscience, 2016
Background: Ischemic brain injury is among the most common causes of death and disability in humans worldwide. Recent findings suggest that neural precursors in the adult mammalian brain can be a therapeutic target in ischemic brain injuries. Curcumin stimulates neurogenesis and reduces oxidative stress in the brain. Objectives: The present study compared the neuroprotective effects of different concentrations of curcumin in various regions of the brain in a rat model of transient global ischemia (TGI). Materials and Methods: Forty-eight adult male Wistar rats were randomly chosen as control, sham (animals only underwent TGI), treatment (100 and 300 mg/kg curcumin following TGI), and vehicle groups. The animals underwent global ischemia imposed by a 20 minute ligation of the bilateral common carotid arteries. Cell death and apoptosis in different areas of brain were evaluated after 3 or 4 weeks by Nissl staining and TUNEL assay respectively. Results: The number of dark neurons and apoptotic cells significantly increased after TGI. The number of TUNEL-positive cells after TGI was significantly higher in the temporal neocortex than in different regions within the hippocampus. Treatment with curcumin at a high dose reduced the numbers of dark neurons and apoptotic cells. Lower concentrations of curcumin showed a neuroprotective effect in the neocortex, whereas higher doses prevented cell death and apoptosis in the neocortex and in different regions of the hippocampus. Conclusions: Regional differences were evident with respect to the neuroprotective effects of curcumin in the temporal cortex and in the different parts of hippocampus following TGI. Further studies are needed to explore the mechanisms underlying these regional differences.
Brain and Behavior, 2017
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 defi...
Turkish Neurosurgery, 2016
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.
Curcumin Provides Neuroprotection After Spinal Cord Injury
Journal of Surgical Research, 2011
Background. Traumatic spinal cord injury (SCI) is a major cause of long-term disability. However, therapeutic agents targeting SCI are sorely lacking. The aim of this study was to investigate whether curcumin has neuroprotective effects after SCI in rats.
The Role of Curcumin in Post-Ischemic Brain
Cerebral Ischemia, 2021
Progressive accumulation of misfolded amyloid and tau protein in intracellular and extracellular spaces is the most crucial etiopathological feature of brain ischemia, synaptic damage, or neural communication impairment. Clinical data suggest that dietary intake of curcumin enhances neurogenesis and offers neuroprotection. Curcumin is a natural polyphenolic compound with diverse and attractive biological properties. It may prevent aging-associated changes in cellular proteins, such as β-amyloid peptide and tau protein, that lead to protein insolubility and aggregation after ischemic brain damage. Therefore, curcumin seems to be a promising supplementary agent against neurodegeneration development after brain ischemia. The aim of this chapter is to highlight our current understanding of the neuroprotective role of curcumin in cerebral ischemia-reperfusion injury. The limitations and adverse events of curcumin are also presented.