Neuroprotective effects of polyhydroxy pregnane glycoside isolated from Wattakaka volubilis (L.f.) Stapf. after middle cerebral artery occlusion and reperfusion in rats

Jadhav, R. S.; Ahmed, Liyakat; Swamy, Paramjyoti L; Sanaullah, Syed

doi:10.1016/j.brainres.2013.02.043

Cited by 13 publications

(10 citation statements)

References 45 publications

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“…NO levels were significantly higher in our I/R group than the control and I/R + minocycline groups, which was supported by others [48,49]. Altas et al [35] reported a nonsignificant increase in NO levels.…”

Section: Discussionsupporting

confidence: 78%

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Aras¹,

Urfalı²,

Serarslan³

et al. 2013

Pediatr Neurosurg

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The aim of this study was to assess the effects of minocycline on cerebral ischemia-reperfusion (I/R) injury in rats. The study was carried out on 24 male Wistar albino rats, weighing 200-250 g, which were divided into three groups: (i) control (n = 8), (ii) I/R (n = 8) and (iii) I/R + minocycline (n = 8). Minocycline was administrated at a dose of 90 mg/kg p.o. to the I/R group 48, 24 and 1 h before ischemia. Following bilateral exposure of the common carotid arteries by anterior cervical dissection and separation of the vagus nerve, I/R injury was performed by occlusion. Following reperfusion, malondialdehyde (MDA), superoxide dismutase, glutathione peroxidase and catalase levels in the blood and brain tissue, and creatine kinase (CK), CK-BB, lactate dehydrogenase (LDH), neuron-specific enolase (NSE) and protein S100β levels in the blood were measured and the histopathological changes were monitored. Regarding histopathological evaluation, symptoms of degeneration were significantly improved in the I/R + minocycline group compared to the I/R-only group. Statistical analysis of the biochemical parameters revealed significant differences in MDA (p < 0.001), nitric oxide (p < 0.05), CK (p < 0.05) and CK-MB (p < 0.05) levels between the I/R + minocycline group and the I/R group. According to the literature, the effect of minocycline is firstly assessed by LDH, CK-MB, NSE and S-100β analysis in addition to antioxidant status and histopathological analysis.

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Section: Discussionsupporting

confidence: 78%

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Aras¹,

Urfalı²,

Serarslan³

et al. 2013

Pediatr Neurosurg

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“…I/R is causal in vascular dementia resulting from cardiovascular or neurosurgery, cardiac or respiratory arrest, and seizures. Nearly one-third of patients with acute ischemic stroke develop early neurological deterioration, a situation associated with increased mortality and morbidity [2,3]. Multiple major pathological mechanisms of I/R, including excytotoxicity, ionic imbalance, oxidative stress, inflammation, and apoptosis [4,5], have been implicated.…”

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confidence: 99%

Neuroprotection of Total Steroid Saponins from Dioscorea zingiberensis against Transient Focal Cerebral Ischemia-Reperfusion Injury in Rats via Anti-Inflammatory and Antiapoptotic Effects

et al. 2014

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Total steroid saponins isolated from Dioscorea zingiberensis have shown a variety of beneficial bioactivities. However, there are no reports about their neuroprotective effects, until now. Therefore, in the present study, we explored the neuroprotective effects of the total steroid saponins from D. zingiberensis on rats against transient focal cerebral ischemia-reperfusion and their underlying mechanisms. Healthy adult Sprague-Dawley rats were randomly assigned to six groups. After pretreatment with D. zingiberensis total steroid saponins intragastrically for six days, the rats were subjected to an ischemia injury by surgery on the middle cerebral artery occlusion for 90 min. Compared to the ischemia-reperfusion group, the D. zingiberensis total steroid saponin group of rats, especially those given a 30-mg/kg dose, showed not only a marked reduction in neurological deficit scores, cerebral infarct volume, and brain edema, but also an increase in neuron survival (Nissl bodies) in the hippocampal cornuammons 1 and cortex hemisphere of the ipsilateral ischemia. At the same time, the inflammatory cytokines in serum induced by the middle cerebral artery occlusion were significantly decreased by the preadministration of D. zingiberensis total steroid saponins. Furthermore, the increase of caspase-3 was evidently reduced in the hippocampal cornuammons 1 and cortex of the hemisphere injured brain. Finally, the downregulating antiapoptotic Bcl-2 and upregulating proapoptotic Bax proteins were obviously suppressed. Taken together, the current findings suggest that D. zingiberensis total steroid saponins played a potential neuroprotective role against a severe injury induced by transient focal cerebral ischemic reperfusion in a rat experimental model, and this role may be mediated by its anti-inflammatory and antiapoptotic actions.

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“…MDA, SOD and NOS are sensitive indicators for evaluating oxidative stress. These factors are activated following acute ischemic or hypoxic injury in the brain, which triggers inflammation and apoptosis and induces a series of brain injuries, including blood-brain-barrier destruction (28-30). In the present study, it was demonstrated that GL inhibited the expression of HMGB1 and RAGE and their downstream inflammatory factors following thrombectomy, and inhibited the expression of MDA, SOD and NOS.…”

Section: Discussionmentioning

confidence: 99%

Effect of HMGB1 and RAGE on brain injury and the protective mechanism of glycyrrhizin in intracranial‑sinus occlusion followed by mechanical thrombectomy recanalization

Dang

Fan

et al. 2019

Int J Mol Med

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The key to successful treatment of cerebral venous-sinus occlusion (CVO) is the rapid recanalization of the sinus following venous-sinus occlusion; however, rapid recanalization of the sinus may also cause secondary cerebral injury. The present study examined mechanical thrombectomy-related brain injury and the possible molecular mechanisms following CVO recanalization, and investigated the protective effect of glycyrrhizin (GL) in CVO recanalization. The cerebral venous sinus thrombosis (CVST) model was induced in rats using 40% FeCl 3 . Mechanical thrombectomy was performed at 6 h post-thrombosis. GL was administered to rats following thromboembolism. Neurological function and brain water content were measured prior to sacrifice of the rats. Serum malondialdehyde, superoxide dismutase and nitric-oxide synthase concentrations were measured. The expression levels of high-mobility group box 1 (HMGB1) and receptor of advanced glycation end products (RAGE) and its downstream inflammatory mediators were measured in serum and brain tissues. Rapid CVO recanalization caused brain injury, and the brain parenchymal damage and neurological deficits caused by CVO were not completely restored following recanalization. Similarly, following rapid recanalization in the venous sinus, the expression levels of HMGB1 and RAGE were lower than those in the CVST group, but remained significantly higher than those of the sham group. The combination of mechanical thrombectomy and GL improved cerebral infarction and cerebral edema in rats, and inhibited the extracellular transport of HMGB1, and the expression of downstream inflammatory factors and oxidative-stress products. The administration of exogenous recombinant HMGB1 reversed the neural protective effects of GL. In conclusion, mechanical thrombectomy subsequent to CVO in rats can cause brain injury following recanalization. HMGB1 and RAGE promote inflammation in the process of brain injury following recanalization. GL has a relatively reliable neuroprotective effect on brain injury by inhibiting HMGB1 and its downstream inflammatory factors, and decreasing oxidative stress.

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Neuroprotective effects of polyhydroxy pregnane glycoside isolated from Wattakaka volubilis (L.f.) Stapf. after middle cerebral artery occlusion and reperfusion in rats

Cited by 13 publications

References 45 publications

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Protective Effects of Minocycline against Short-Term Ischemia-Reperfusion Injury in Rat Brain

Neuroprotection of Total Steroid Saponins from Dioscorea zingiberensis against Transient Focal Cerebral Ischemia-Reperfusion Injury in Rats via Anti-Inflammatory and Antiapoptotic Effects

Effect of HMGB1 and RAGE on brain injury and the protective mechanism of glycyrrhizin in intracranial‑sinus occlusion followed by mechanical thrombectomy recanalization

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