Cerebral ischemia/reperfusion (I/R) injury causes cognitive deficits, excitotoxicity, neuroinflammation, oxidative stress and brain edema. Vitamin K2 (Menaquinone 4, MK-4) as a potent antioxidant can be a good candidate to ameliorate I/R consequences. This study focused on the neuroprotective effects of MK-4 for cerebral I/R insult in rat's hippocampus. The rat model of cerebral I/R was generated by transient bilateral common carotid artery occlusion for 20 min. Rats were divided into control, I/R, I/R+DMSO (solvent (1% v/ v)) and I/R+MK-4 treated (400 mg/kg, i.p.) groups. Twenty-four hours after I/R injury induction, total brain water content, superoxide dismutase (SOD) activity, nitrate/nitrite concentration and neuronal density were evaluated. In addition to quantify the apoptosis processes, TUNEL staining, as well as expression level of Bax and Bcl2, were assessed. To evaluate astrogliosis and induced neurotoxicity by I/R GFAP and GLT-1 mRNA expression level were quantified. Furthermore, pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α were measured. Seven days post I/R, behavioral analysis to quantify cognitive function, as well as Nissl staining for surviving neuronal evaluation, were conducted. The findings indicated that administration of MK-4 following I/R injury improved anxiety-like behavior, short term and spatial learning and memory impairment induced by I/R. Also, MK-4 was able to diminish the increased total brain water content, apoptotic cell density, Bax/ Bcl2 ratio and GFAP mRNA expression following I/R. In addition, the high level of nitrate/nitrite, IL-6, IL-1β and TNF-α induced by I/R was reduced after MK-4 administration. However, MK-4 promotes the level of SOD activity and GLT-1 mRNA expression in I/R rat model. The findings demonstrated that MK-4 can rescue transient global cerebral I/R consequences via its anti-inflammatory and anti-oxidative stress features. MK-4 administration ameliorates neuroinflammation, neurotoxicity and neuronal cell death processes and leads to neuroprotection. PLOS ONEPLOS ONE | https://doi.org/10.1371/journal.pone.0229769 March 9, 2020 1 / 30 OPEN ACCESS Citation: Farhadi Moghadam B, Fereidoni M (2020) Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat. PLoS ONE 15(3): e0229769. https://
Aims: One of the most basic methods for coping with diseases and pain relief had been the use of medicinal plants. The aim of this study was to the determination of analgesic and anti-inflammatory effects of Salvia multicaulis hydroalcoholic extract. Materials & Methods: In this experimental study, 42 male Wistar rats were divided in 6 groups (n=7); the control (receive nothing), the sham (receive solvent intraperitoneally) and 4 groups that received plant extract at the doses of 50, 100, 200 and 400mg/kg intraperitoneally. Tail flick and formalin test were used for evaluation of thermal and chemical pain, also for assessment the degree of inflammation, rat paw edema volume was acquired by plethysmometric test. Data were analyzed in SPSS 16 software by ANOVA with repeated measuring and T student tests. Findings: The intraperitoneally injection of extract in all doses decreased the chemical pain induced by formalin (p<0.05). Hydroalcoholic extract of plant at doses 200 and 400mg/kg caused hyperalgesia in compared with control group (p<0.01). All concentrations of hydroalcoholic extract of plant decreased the inflammation (p<0.01). Conclusion: Intraperitoneally administration of hydroalcoholic extract of Salvia multicaulis has analgesic effects.
Objectives Cerebral ischemia-reperfusion leads to brain tissue injury. Inflammation and apoptosis play pivotal roles in the pathology. α-Pinene is an organic compound of many aromatic plants and is known as a potent agent to possess antioxidant, and anti-inflammatory properties. Here, we sought to identify the anti-inflammatory and anti-apoptosis mechanism by which α-Pinene improves brain ischemia injury. Methods Male Wistar rats underwent MCAO surgery for 1 hour and different doses of alpha-pinene (25, 50, and 100 mg/kg) were intraperitoneally injected immediately after reperfusion to test this hypothesis. IV, NDS, gene and protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB) p65, and caspase-3 were assessed 24h after reperfusion. Key findings Results demonstrated that NF-κB p65, iNOS, and COX-2 gene and protein expression increased in the hippocampus, cortex, and striatum after 24 h of reperfusion, and alpha-pinene significantly inhibited NF-kB p65, iNOS, and COX-2 expression. Also, alpha-pinene significantly reduced the ischemia/reperfusion-induced caspase-3 activation in CA1 area of hippocampus. Conclusions Results showed that alpha-pinene protects the cerebral against ischemic damage caused by MCAO, and this effect may be through the regulating iNOS -NF-kappa B- COX-2 and caspas-3 inflammatory and apoptotic pathways.
Introduction:Cerebral ischemia results from glucose and oxygen reduction following insufficiency of brain blood supply. Ischemia could be induced in focal and diffuse models.A type of animal model of transient brain global ischemia is induced via common carotid arteries ligation and focal ischemia is induced by middle cerebral artery obstructions, which are the most common approach for investigation of the pathophysiology of brain ischemia and its mechanisms. Understanding of pathophysiological mechanisms of cerebral ischemia is important for the development of novel preventive and therapeutic approaches for brain ischemia. Conclusion: In the present study, we have described the pathophysiological mechanisms of brain ischemic events, such as decreases in cerebral blood flow, glutamate neurotoxicity, oxidative stress, inflammation, brain edema, cholinergic system dysfunction, neural cell death, and hippocampal damage. Extensive efforts are being performed to find effective drugs with the least side effects for the modulation of pathways involved in brain ischemia. In summation, represented information may be an appropriate guide to design novel therapeutic strategies for brain ischemia.a
Objectives Cerebral ischemia-reperfusion leads to brain tissue injury. Inflammation and apoptosis play pivotal roles in the pathology. α-Pinene is an organic compound of many aromatic plants and is known as a potent agent to possess antioxidant, and anti-inflammatory properties. Here, we sought to identify the anti-inflammatory and anti-apoptosis mechanism by which α-Pinene improves brain ischemia injury. Methods Male Wistar rats underwent MCAO surgery for 1 hour and different doses of alpha-pinene (25, 50, and 100 mg/kg) were intraperitoneally injected immediately after reperfusion to test this hypothesis. IV, NDS, gene and protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB) p65, and caspase-3 were assessed 24h after reperfusion. Key findings Results demonstrated that iNOS, COX2 and NF-KB gene and protein expression increased in the hippocampus, cortex, and striatum after 24 h of reperfusion, and alpha-pinene significantly inhibited iNOS, COX2 and NF-KB expression. Also, alpha-pinene significantly reduced the ischemia/reperfusion-induced caspase-3 activation in CA1 area of hippocampus. Conclusions Results showed that alpha-pinene protects the cerebral against ischemic damage caused by MCAO, and this effect may be through the regulating iNOS, COX2 and NF-KB and caspas-3 inflammatory and apoptotic pathways.
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