Effect of Combination Treatment of Candesartan and Curcumin on Traumatic Brain Injury in Mice (original) (raw)
Related papers
Open Access Macedonian Journal of Medical Sciences, 2020
BACKGROUND: Traumatic brain injury (TBI) is the most common problem that caused morbidity and mortality in the world. Secondary brain injury is a complex cascade that causes brain cell apoptosis. Curcumin is a natural product that has neuroprotective properties. AIM: This study aimed to investigate the effect of curcumin toward heat shock protein 70 (HSP 70) expression against the expression apoptosis marker (apoptosis-inducing factor [AIF], caspase-3, and TUNEL assay) in brain tissue after TBI. METHODS: Thirty-three Sprague Dawley rats were randomized into three treatment groups, that is, sham-operated controls, closed head trauma (CHT), and CHT with curcumin extract (treatment group). In the treatment group, curcumin was given 500 mg/kg per oral for 7 days, then brain tissues were investigated (marker AIF, caspase-3, TUNEL assay, and HSP 70) through immunohistochemistry. Statistical test using one-way ANOVA test and Tukey honestly significant difference as post hoc test. RESULTS: ...
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.
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.
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.
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...
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.
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.
World neurosurgery, 2016
The development of secondary brain injury via oxidative stress after traumatic brain injury (TBI) is well known. Decorin inactivates Transforming growth factor-β1 (TGF-β1), complement system (CS) and Tumor necrosis factor-α (TNF-α) which are related the oxidative stress and apoptosis. Consequently, the aim of the present study was to evaluate the role of Decorin (DC) on TBI. A total of 24 male rats were used and divided into four groups as follows; control, trauma, DC, and methylprednisolone (MP). The trauma, DC and MP groups were subjected to closed-head contusive weight-drop injuries. Rats received treatment with intraperitoneally (IP) saline, DC or MP respectively. All the animals were sacrificed at the 24th hour after trauma and brain tissues were extracted. The oxidant/antioxidant parameters [malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), nitric oxide (NO)] and caspase-3 in the cerebral tissue were analyzed, and histomorphological evaluation of...
Behavioural Brain Research, 2008
Curcumin (diferuloylmethane), an active ingredient of turmeric, obtained from the powdered rhizomes of Curcuma longa Linn., has been traditionally recognized for treatment of several diseases. To evaluate the potential clinical use of curcumin, we determined the dose dependence of its effects in the therapeutic window and of the neuroprotective efficacy in a cerebral thromboembolic model of the rat. Rats were subjected to occlusion of the middle cerebral artery (MCAo) by a thrombus and treated with different doses of curcumin or the vehicle at 4 h after ischemia. The animals were assessed after 24 h for motor performance and neurological deficit. The rats were sacrificed immediately afterwards for evaluation of infarct, edema volume, estimation of nitrate and nitrite levels, neutrophil infiltration and levels of GSH and glutathione peroxidase (GSH-Px) in brain tissue. Curcumin reduced in a dose-dependent manner the ischemia-induced cerebral infarct and edema volume and attenuated neurological deficits observed after 24 h. Curcumin reduced post-ischemic brain neutrophil infiltration, nitrate and nitrite levels and ameliorated the loss of GSH-Px and tends to increase the GSH levels but not significantly in the brain tissue. Neuronal levels of reactive oxygen species, peroxynitrite, and nitric oxide were lowered and in brain cryosections inducible nitric oxide synthase expression were significantly inhibited after treatment with curcumin. The present study is the first evidence of effectiveness of curcumin when given 4 h postischemia in the rat thromboembolic stroke models, as it reduces infarct volume, ameliorates the sensory motor function and significantly attenuated the nitrosative stress.