Middle Cerebral Artery Occlusion (MCAO) https://greenmedinfo.com/taxonomy/term/5080/all en Acorus calamus has a neuroprotective effect against middle cerebral artery occlusion-induced ischaemia in rat. https://greenmedinfo.com/article/acorus-calamus-has-neuroprotective-effect-against-middle-cerebral-artery-occlu PMID:  Hum Exp Toxicol. 2006 Apr;25(4):187-94. PMID: 16696294 Abstract Title:  Neuroprotective effect of Acorus calamus against middle cerebral artery occlusion-induced ischaemia in rat. Abstract:  The neuroprotective potential of ethanol:water (1:1) extract of rhizomes of Acorus calamus (AC-002) has been investigated in middle cerebral artery occlusion (MCAO)-induced ischaemia in rats. A significant behavioural impairment in Rota-Rod performance and grid walking was observed in rats, 72 hours after MCAO as compared to sham-operated animals. These rats also exhibited an increase in lipid peroxidation (cortex -157%, corpus striatum - 58%) and a decrease in glutathione levels (cortex - 59%, corpus striatum - 34%) and superoxide dismutase (SOD) activity (cortex - 64%, corpus striatum - 32%) as compared to sham-operated animals. Ischaemic rats treated with AC-002 (25 mg/kg, p.o.) exhibited a significant improvement in neurobehavioural performance viz. Rota-Rod performance and grid walking as compared to the MCAO group. Interestingly, treatment with AC-002 in MCAO rats significantly decreased malonaldialdehyde levels in cortex as compared to ischaemic rats. A significant increase in reduced glutathione levels and SOD activity was also observed both in cortex and corpus striatum in MCAO rats treated with AC-002 in comparison to MCAO rats. Treatment with AC-002 in MCAO rats also reduced the contralateral cortical infarct area (19%) as compared to MCAO rats (33%). Neurological function score was improved in the AC-002-treated rats as compared to the MCAO group. The results of the present study indicate the neuroprotective efficacy of A. calamus in the rat model of ischaemia. https://greenmedinfo.com/article/acorus-calamus-has-neuroprotective-effect-against-middle-cerebral-artery-occlu#comments Acorus calamus Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Plant Extracts Animal Study Thu, 28 Jan 2010 14:39:54 +0000 greenmedinfo 50350 at https://greenmedinfo.com Acupuncture attenuates neuronal cell death in middle cerebral artery occlusion model of focal ischemia. https://greenmedinfo.com/article/acupuncture-attenuates-neuronal-cell-death-middle-cerebral-artery-occlusion-mo PMID:  Neurol Res. 2010 Feb;32 Suppl 1:84-7. PMID: 20034452 Abstract Title:  Acupuncture attenuates neuronal cell death in middle cerebral artery occlusion model of focal ischemia. Abstract:  OBJECTIVES: This study was designed to investigate the neuroprotective effect of acupuncture in the middle cerebral artery occlusion-induced ischemia model. METHODS: Sprague-Dawley rats were randomly divided into two experimental groups: middle cerebral artery occlusion group (MCAO, n=8), and middle cerebral artery occlusion plus acupuncture group (MCAO + Acu, n=8). Acupuncture stimulation was given immediately after reperfusion. The effect of its stimulation to both GB34 and GB39 on the size of the brain infarct and the functional status of the brain cells after middle cerebral artery occlusion was examined by nissl staining and neuron-specific nuclear protein immunohistochemistry. RESULTS: The infarction volume was significantly decreased in the MCAO + Acu group (16.4 +/- 4.8%), compared with the MCAO group (39.9 +/- 10.2%). The number of neuron-specific nuclear protein-positive cells in the MCAO group was significantly decreased by 42.3 +/- 12.6% in the striatum and by 45.8 +/- 5.8% in the motor cortex, but the neuron-specific nuclear protein-positive cells in the MCAO + Acu group were rescued by 67.0 +/- 3.8% in the striatum and by 68.1 +/- 4.5% in the motor cortex, compared with the contralateral side (100%). DISCUSSION: This study showed that acupuncture had neuroprotective effects against focal ischemia in the middle cerebral artery occlusion model. https://greenmedinfo.com/article/acupuncture-attenuates-neuronal-cell-death-middle-cerebral-artery-occlusion-mo#comments Middle Cerebral Artery Occlusion (MCAO) Acupuncture Neuroprotective Agents Animal Study Mon, 08 Feb 2010 15:31:20 +0000 greenmedinfo 50979 at https://greenmedinfo.com Anti-neuroinflammatory effect of alantolactone through the suppression of the NF-κB and MAPK signaling pathways. https://greenmedinfo.com/article/anti-neuroinflammatory-effect-alantolactone-through-suppression-nf-b-and-mapk- PMID:  Cells. 2019 07 18 ;8(7). Epub 2019 Jul 18. PMID: 31323885 Abstract Title:  Anti-Neuroinflammatory Effect of Alantolactone through the Suppression of the NF-κB and MAPK Signaling Pathways. Abstract:  Neuroinflammation is a major cause of central nervous system (CNS) damage and can result in long-term disability and mortality. Therefore, the development of effective anti-neuroinflammatory agents for neuroprotection is vital. To our surprise, the naturally occurring molecule alantolactone (Ala) was reported to significantly inhibit tumor growth and metastasis as a result of its excellent anti-inflammatory effects. Thus, we proposed that it could also act as an anti-neuroinflammatory agent. Thus, in this study, a coculture system of BV2 cells and PC12 cells were used as an in vitro neuroinflammatory model to investigate the anti-neuroinflammatory mechanism of Ala. The results indicated that Ala downregulated the expression of proinflammatory factors by suppressing the nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. Further evaluation using a middle cerebral artery occlusion and reperfusion (MCAO/R) rat model supported the conclusion that Ala could (1) alleviate cerebral ischemia-reperfusion injury; (2) reduce neurological deficits, cerebral infarct volume, and brain edema; and (3) attenuate the apoptosis and necrosis of neurons. In sum, Ala demonstrates anti-neuroinflammatory properties that contribute to the amelioration of CNS damage, and it could be a promising candidate for future applications in CNS injury treatment. <p><a href="https://greenmedinfo.com/article/anti-neuroinflammatory-effect-alantolactone-through-suppression-nf-b-and-mapk-" target="_blank">read more</a></p> https://greenmedinfo.com/article/anti-neuroinflammatory-effect-alantolactone-through-suppression-nf-b-and-mapk-#comments Brain Inflammation Elecampane Middle Cerebral Artery Occlusion (MCAO) Anti-Inflammatory Agents Neuroprotective Agents NF-kappaB Inhibitor Animal Study Fri, 01 Oct 2021 23:18:44 +0000 greenmedinfo 246609 at https://greenmedinfo.com Apigenin may play an important neuroprotective role in acute transient focal cerebral ischemia-reperfusion injury in rats. https://greenmedinfo.com/article/apigenin-may-play-important-neuroprotective-role-acute-transient-focal-cerebra PMID:  Zhong Yao Cai. 2008 Jun;31(6):870-3. PMID: 18998572 Abstract Title:  [Neuroprotective effects of apigenin on acute transient focal cerebral ischemia-reperfusion injury in rats]. Abstract:  OBJECTIVE: To evaluate the neuroprotective effects of apigenin on acute transient focal cerebral ischemia-reperfusion injury in rats. METHODS: The acute transient focal cerebral ischemia-reperfusion model was established with modified method of insertion of thread fish nylon into and staying for two hours and then withdrawing from middle cerebral artery in rats. In experiment groups the neurological behavior scores, TTC stain of brain slices, neurocyte morphology were observed, and brain water content and Evans blue (EB) content were measured. RESULTS: Abnormal neurological behavior scores were existed in apigenin-treated group and model group. Typical cortical infarct lesions in model group were found by TTC stain. The neurocyte morphology in model group 4 hours was found in swollen glia and obvious edema near capillary and within nervous process, and karyopycnosis in neuron of ischemic cortex and hippocampus CA1 under electric microscope. However lesion was alleviated in apigenin-treated group. The brain water content and EB content in apigenin-treated group were lower than model group. CONCLUSION: Apigenin may play an important neuroprotective role in acute transient focal cerebral ischemia-reperfusion injury in rats. https://greenmedinfo.com/article/apigenin-may-play-important-neuroprotective-role-acute-transient-focal-cerebra#comments Apigenin Cerebral Ischemia Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Animal Study Fri, 19 Feb 2010 15:18:01 +0000 greenmedinfo 51872 at https://greenmedinfo.com Astaxanthin has neuroprotective properties in an animal model of focal cerebral artery occlusion. https://greenmedinfo.com/article/astaxanthin-has-neuroprotective-properties-animal-model-focal-cerebral-artery- PMID:  Brain Res. 2010 Nov 11;1360:40-8. Epub 2010 Sep 21. PMID: 20846510 Abstract Title:  Neuroprotective effect of astaxanthin on H(2)O(2)-induced neurotoxicity in vitro and on focal cerebral ischemia in vivo. Abstract:  Astaxanthin (AST) is a powerful antioxidant that occurs naturally in a wide variety of living organisms. Much experimental evidence has proved that AST has the function of eliminating oxygen free radicals and can protect organisms from oxidative damage. The present study was carried out to further investigate the neuroprotective effect of AST on oxidative stress induced toxicity in primary culture of cortical neurons and on focal cerebral ischemia-reperfusion induced brain damage in rats. AST, over a concentration range of 250-1000nM, attenuated 50μM H(2)O(2)-induced cell viability loss. 500nM AST pretreatment significantly inhibited H(2)O(2)-induced apoptosis measured by Hoechst 33342 staining and restored the mitochondrial membrane potential (MMP) measured by a fluorescent dye, Rhodamine 123. In vivo, AST prevented cerebral ischemic injuryinduced by 2h middle cerebral artery occlusion (MCAO) and 24h reperfusion in rats. Pretreatment of AST intragastrically twice at 5h and 1h prior to ischemia dramatically diminished infarct volume and improved neurological deficit in a dose-dependent manner. Nissl staining showed that the neuronal injury was significantly improved by pretreatment of AST at 80mg/kg. Taken together, these results suggest that pretreatment with AST exhibits noticeable neuroprotection against brain damage induced by ischemia-reperfusion and the antioxidant activity of AST maybe partly responsible for it. https://greenmedinfo.com/article/astaxanthin-has-neuroprotective-properties-animal-model-focal-cerebral-artery-#comments Astaxanthin Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Animal Study Tue, 28 Jun 2011 22:18:43 +0000 greenmedinfo 65022 at https://greenmedinfo.com Astragaloside IV attenuates cerebral ischemia and reperfusion injury. https://greenmedinfo.com/article/astragaloside-iv-attenuates-cerebral-ischemia-and-reperfusion-injury PMID:  Sheng Li Xue Bao. 2019 Jun 25 ;71(3):424-430. PMID: 31218333 Abstract Title:  [Astragaloside IV attenuates cerebral ischemia and reperfusion injury and reduces activation of NLRP3 inflammasome and NF-κB phosphorylation in rats following a transient middle cerebral artery occlusion]. Abstract:  The present study was aimed to investigate the protective effect and anti-inflammation mechanism of astragaloside IV (AST-IV) on cerebral ischemia and reperfusion injury. Following the establishment of cerebral ischemia and reperfusion model in rats by modified suture method, neurological deficit scores and cerebral infarct volume were used to evaluate the pharmacological effect of AST-IV against cerebral ischemia-reperfusion injury. Western blot was used to detect the expression levels of NLRP3, pro-Caspase-1, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18, IL-18, phosphorylated and total nuclear factor kappa B (NF-κB)/p65 protein in the brain tissue. The results showed that compared with model group, the intervention of AST-IV decreased the neurological deficit scores, reduced the cerebral infarct volume, decreased the levels of NLRP3, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18 and IL-18, and inhibited the expression of phosphorylated NF-κB in brain tissue. The results suggest that AST-IV has a protective effect against cerebral ischemia and reperfusion injury, and its mechanism is related to inhibiting the phosphorylationof NF-κB and NLRP3 inflammasome activation. <p><a href="https://greenmedinfo.com/article/astragaloside-iv-attenuates-cerebral-ischemia-and-reperfusion-injury" target="_blank">read more</a></p> https://greenmedinfo.com/article/astragaloside-iv-attenuates-cerebral-ischemia-and-reperfusion-injury#comments Astragaloside Brain Ischemia Middle Cerebral Artery Occlusion (MCAO) Anti-Inflammatory Agents Interleukin-1 beta downregulation NF-kappaB Inhibitor In Vitro Study Mon, 28 Oct 2019 18:38:24 +0000 greenmedinfo 200326 at https://greenmedinfo.com Berberine exhibits neuroprotective qualities against ischemic brain damage in stroke models https://greenmedinfo.com/article/berberine-exhibits-neuroprotective-qualities-against-ischemic-brain-damage-str PMID:  Neurosci Lett. 2008 Dec 5 ;447(1):31-6. Epub 2008 Sep 30. PMID: 18838103 Abstract Title:  Neuroprotective effects of berberine on stroke models in vitro and in vivo. Abstract:  Berberine is an alkaloid derived from herb medicine Coptidis Rhizom. Although there are increasing evidences that berberine exhibits neuroprotective effects against ischemic brain damage, little is known about the mechanism. In this study, we investigated the effect of berberine on ischemic injury in a middle cerebral artery occlusion (MCAO) model. We found that berberine improved neurological outcome and reduced ischemia/reperfusion (I/R)-induced cerebral infarction 48h after MCAO. The protective effect of berberine was confirmed in in vitro study. Berberine protected PC12 cells against oxygen-glucose deprivation (OGD)-induced injury. The results showed that berberine inhibited reactive oxygen species (ROS) generation, and subsequent release of pro-apoptotic factor cytochrome c and apoptosis-inducing factors (AIFs) evoked by OGD. Findings of this study suggest that berberine protects against ischemic brain injury by decreasing the intracellular ROS level and subsequently inhibiting mitochondrial apoptotic pathway. https://greenmedinfo.com/article/berberine-exhibits-neuroprotective-qualities-against-ischemic-brain-damage-str#comments Berberine Brain Ischemia Hypoxia Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Ischemia Reperfusion Injury Animal Study Sun, 15 Apr 2012 12:17:23 +0000 greenmedinfo 74331 at https://greenmedinfo.com Betulinic acid ameliorates cerebral injury in middle cerebral artery occlusion. https://greenmedinfo.com/article/betulinic-acid-ameliorates-cerebral-injury-middle-cerebral-artery-occlusion PMID:  ACS Chem Neurosci. 2021 Jul 23. Epub 2021 Jul 23. PMID: 34296845 Abstract Title:  Betulinic Acid Ameliorates Cerebral Injury in Middle Cerebral Artery Occlusion Rats through Regulating Autophagy. Abstract:  Cerebral ischemic stroke (CIS) is an acute cerebrovascular disease that is caused by the sudden rupture of blood vessels inside the brain and the intervention of reperfusion to the brain, resulting in severe cerebral injury. Autophagy has been reported to be involved in the occurrence and progression of CIS. Betulinic acid (BA) is a pentacyclic triterpene acid mainly extracted from birch bark. Studies have shown the neuroprotective effects of BA. Here, the effect and mechanism of BA on ischemia-reperfusion induced cerebral injury was explored using a CIS model in vivo via 1 h middle cerebral artery occlusion (MCAO) and 24 h reperfusion in rats and in vitro via oxygen-glucose deprivation/reperfusion (OGD/R) of PC12 cells, respectively. We found that BA not only reduced cerebral injury by reducing oxidative stress but also activated the SIRT1/FoxO1 pathway to suppress autophagy and improve cerebral injury in MCAO rats. These results provide a basis for the potential clinical application of BA. <p><a href="https://greenmedinfo.com/article/betulinic-acid-ameliorates-cerebral-injury-middle-cerebral-artery-occlusion" target="_blank">read more</a></p> https://greenmedinfo.com/article/betulinic-acid-ameliorates-cerebral-injury-middle-cerebral-artery-occlusion#comments Betulinic acid Middle Cerebral Artery Occlusion (MCAO) Autophagy Inhibitors Neuroprotective Agents Animal Study In Vitro Study Tue, 27 Jul 2021 17:24:26 +0000 greenmedinfo 243381 at https://greenmedinfo.com Cannabidiol and abnormal cannabidiol reduced the infarct volume. https://greenmedinfo.com/article/cannabidiol-and-abnormal-cannabidiol-reduced-infarct-volume n/a PMID:  Stroke. 2005 May ;36(5):1077-82. Epub 2005 Apr 21. PMID: 15845890 Abstract Title:  Cannabidiol prevents cerebral infarction via a serotonergic 5-hydroxytryptamine1A receptor-dependent mechanism. Abstract:  BACKGROUND AND PURPOSE: Cannabidiol has been reported to be a neuroprotectant, but the neuroprotective mechanism of cannabidiol remains unclear. We studied the neuroprotective mechanism of cannabidiol in 4-hour middle cerebral artery (MCA) occlusion mice. METHODS: Male MCA occluded mice were treated with cannabidiol, abnormal cannabidiol, anandamide, methanandamide, cannabidiol plus capsazepine, and cannabidiol plus WAY100135 before and 3 hours after MCA occlusion. The infarct size was determined after 24 hours (2,3,5-triphenyltetrazolium chloride staining). Cerebral blood flow (CBF) was measured at, before and 1, 2, 3, and 4 hours after MCA occlusion. RESULTS: Cannabidiol significantly reduced the infarct volume induced by MCA occlusion in a bell-shaped curve. Similarly, abnormal cannabidiol but not anandamide or methanandamide reduced the infarct volume. Moreover, the neuroprotective effect of cannabidiol was inhibited by WAY100135, a serotonin 5-hydroxytriptamine1A (5-HT1A) receptor antagonist but not capsazepine a vanilloid receptor antagonist. Cannabidiol increased CBF to the cortex, and the CBF was partly inhibited by WAY100135 in mice subjected to MCA occlusion. CONCLUSIONS: Cannabidiol and abnormal cannabidiol reduced the infarct volume. Furthermore, the neuroprotective effect of cannabidiol was inhibited by WAY100135 but not capsazepine, and the CBF increased by cannabidiol was partially reversed by WAY100135. These results suggested that the neuroprotective effect of cannabidiol may be related to the increase in CBF through the serotonergic 5-HT1A receptor. https://greenmedinfo.com/article/cannabidiol-and-abnormal-cannabidiol-reduced-infarct-volume#comments Cannabidiol Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Cannabidiol Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Animal Study Fri, 09 Jun 2017 23:16:16 +0000 greenmedinfo 148983 at https://greenmedinfo.com Cannabidiol prevents infarction via the non-CB1 cannabinoid receptor mechanism https://greenmedinfo.com/article/cannabidiol-prevents-infarction-non-cb1-cannabinoid-receptor-mechanism PMID:  Neuroreport. 2004 Oct 25 ;15(15):2381-5. PMID: 15640760 Abstract Title:  Cannabidiol prevents infarction via the non-CB1 cannabinoid receptor mechanism. Abstract:  Cannabidiol, a non-psychoactive constituent of cannabis, has been reported as a neuroprotectant. Cannabidiol and Delta(9)-tetrahydrocannabinol, the primary psychoactive constituent of cannabis, significantly decreased the infarct volume at 4 h in the mouse middle cerebral artery occlusion model. The neuroprotective effects of Delta(9)-tetrahydrocannabinol but not cannabidiol were inhibited by SR141716, a cannabinoid CB1 receptor antagonist, and were abolished by warming of the animals to the levels observed in the controls. Delta(9)-Tetrahydrocannabinol significantly decreased the rectal temperature, and the hypothermic effect was inhibited by SR141716. These results surely show that the neuroprotective effect of Delta(9)-tetrahydrocannabinol are via a CB1 receptor and temperature-dependent mechanisms whereas the neuroprotective effects of cannabidiol are independent of CB1 blockade and of hypothermia. <p><a href="https://greenmedinfo.com/article/cannabidiol-prevents-infarction-non-cb1-cannabinoid-receptor-mechanism" target="_blank">read more</a></p> https://greenmedinfo.com/article/cannabidiol-prevents-infarction-non-cb1-cannabinoid-receptor-mechanism#comments Cannabidiol Delta-tetrahydrocannabinol (THC) Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents In Vitro Study Mon, 12 Jun 2017 22:25:55 +0000 greenmedinfo 149021 at https://greenmedinfo.com Cannabidiol provides potent and long-lasting neuroprotection through an anti-inflammatory CB1 receptor-independent mechanism. https://greenmedinfo.com/article/cannabidiol-provides-potent-and-long-lasting-neuroprotection-through-anti-infl PMID:  J Neurochem. 2007 Sep ;102(5):1488-96. Epub 2007 Apr 16. PMID: 17437545 Abstract Title:  Delayed treatment with cannabidiol has a cerebroprotective action via a cannabinoid receptor-independent myeloperoxidase-inhibiting mechanism. Abstract:  We examined the neuroprotective mechanism of cannabidiol, non-psychoactive component of marijuana, on the infarction in a 4 h mouse middle cerebral artery (MCA) occlusion model in comparison with Delta(9)-tetrahydrocannabinol (Delta(9)-THC). Release of glutamate in the cortex was measured at 2 h after MCA occlusion. Myeloperoxidase (MPO) and cerebral blood flow were measured at 1 h after reperfusion. In addition, infarct size and MPO were determined at 24 and 72 h after MCA occlusion. The neuroprotective effect of cannabidiol was not inhibited by either SR141716 or AM630. Both pre- and post-ischemic treatment with cannabidiol resulted in potent and long-lasting neuroprotection, whereas only pre-ischemic treatment with Delta(9)-THC reduced the infarction. Unlike Delta(9)-THC, cannabidiol did not affect the excess release of glutamate in the cortex after occlusion. Cannabidiol suppressed the decrease in cerebral blood flow by the failure of cerebral microcirculation after reperfusion and inhibited MPO activity in neutrophils. Furthermore, the number of MPO-immunopositive cells was reduced in the ipsilateral hemisphere in cannabidiol-treated group. Cannabidiol provides potent and long-lasting neuroprotection through an anti-inflammatory CB(1) receptor-independent mechanism, suggesting that cannabidiol will have a palliative action and open new therapeutic possibilities for treating cerebrovascular disorders. <p><a href="https://greenmedinfo.com/article/cannabidiol-provides-potent-and-long-lasting-neuroprotection-through-anti-infl" target="_blank">read more</a></p> https://greenmedinfo.com/article/cannabidiol-provides-potent-and-long-lasting-neuroprotection-through-anti-infl#comments Cannabidiol Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Animal Study Tue, 13 Jun 2017 19:56:50 +0000 greenmedinfo 149054 at https://greenmedinfo.com Cannabidiol will open new therapeutic possibilities for post-ischemic injury via HMGB1-inhibiting mechanism. https://greenmedinfo.com/article/cannabidiol-will-open-new-therapeutic-possibilities-post-ischemic-injury-hmgb1 PMID:  Neuropharmacology. 2008 Dec ;55(8):1280-6. Epub 2008 Jun 27. PMID: 18634812 Abstract Title:  Cannabidiol prevents a post-ischemic injury progressively induced by cerebral ischemia via a high-mobility group box1-inhibiting mechanism. Abstract:  We examined the cerebroprotective mechanism of cannabidiol, the non-psychoactive component of marijuana, against infarction in a 4-h mouse middle cerebral artery (MCA) occlusion model. Cannabidiol was intraperitoneally administrated immediately before and 3h after cerebral ischemia. Infarct size and myeloperoxidase (MPO) activity, a marker of neutrophil, monocyte/macropharge, were measured at 24h after cerebral ischemia. Activated microglia and astrocytes were evaluated by immunostaining. Moreover, high-mobility group box1 (HMGB1) was also evaluated at 1 and 3 days after MCA occlusion. In addition, neurological score and motor coordination on the rota-rod test were assessed at 1 and 3 days after cerebral ischemia. Cannabidiol significantly prevented infarction and MPO activity at 20h after reperfusion. These effects of cannabidiol were not inhibited by either SR141716 or AM630. Cannabidiol inhibited the MPO-positive cells expressing HMGB1 and also decreased the expression level of HMGB1 in plasma. In addition, cannabidiol decreased the number of Iba1- and GFAP-positive cells at 3 days after cerebral ischemia. Moreover, cannabidiol improved neurological score and motor coordination on the rota-rod test. Our results suggest that cannabidiol inhibits monocyte/macropharge expressing HMGB1 followed by preventing glial activation and neurological impairment induced by cerebral ischemia. Cannabidiol will open new therapeutic possibilities for post-ischemic injury via HMGB1-inhibiting mechanism. <p><a href="https://greenmedinfo.com/article/cannabidiol-will-open-new-therapeutic-possibilities-post-ischemic-injury-hmgb1" target="_blank">read more</a></p> https://greenmedinfo.com/article/cannabidiol-will-open-new-therapeutic-possibilities-post-ischemic-injury-hmgb1#comments Cannabidiol Hypertension Middle Cerebral Artery Occlusion (MCAO) Neuroprotective Agents Animal Study Tue, 13 Jun 2017 22:53:34 +0000 greenmedinfo 149083 at https://greenmedinfo.com Cerebral ischemia was protected by oleuropein. https://greenmedinfo.com/article/cerebral-ischemia-was-protected-oleuropein PMID:  Med Sci Monit. 2018 Sep 19 ;24:6587-6598. Epub 2018 Sep 19. PMID: 30230477 Abstract Title:  Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis. Abstract:  BACKGROUND In this study, we investigated the potential neuroprotective effect of oleuropein (OLE) on apoptotic changes via modulating Akt/glycogen synthase kinase 3 beta (Akt/GSK-3b) signaling in a rat model of cerebral ischemia/reperfusion injury (IRI). MATERIAL AND METHODS Sprague-Dawley male rats (12 weeks, n=200) were randomly assigned to 5 groups: sham group, vehicle (IRI+ vehicle) group, OLE (IRI+OLE) group, OLE+LY294002 (IRI+OLE+LY294002) group, and LY294002(IRI+LY294002) group. The rats were subjected to cerebral ischemia/reperfusion injury (IRI) model and treated once daily for 5 days with vehicle and OLE (100 mg/kg via intraperitoneal injection) after IRI injury. LY294002 (0.3 mg/kg) was intraperitoneally injected once at 30 min after IRI injury. Brain edema, neurological deficit, rotarod latencies, and Morris water maze (MWM) performance were evaluated after IRI. The number of dead cells were assayed by TUNEL staining. Western blot was used to detect the expression of Bcl-2, Bax, cleaved caspase-3 (CC3), neurotrophic factors, and the phosphorylation levels of Akt and GSK-3β. RESULTS Compared with the vehicle group, brain water content, neurological deficits, rotarod latencies, and escape latency following IRI were reduced in the OLE group. Cell apoptosis and reduced neurotrophic factor caused by IRI was also attenuated by OLE. Furthermore, increased p-Akt and decreased p-GSK-3β were caused by OLE, which were associated with decrease of Bax/Bcl-2 ratio and the suppression of Caspase-3 activity after IRI. Importantly, all the beneficial effects of OLE in the vehicle group were abrogated by PI3K inhibitor LY294002. CONCLUSIONS Cerebral ischemia was protected byOLE via suppressing apoptosis through the Akt/GSK-3β pathway and upregulating neurotrophic factor after IRI. <p><a href="https://greenmedinfo.com/article/cerebral-ischemia-was-protected-oleuropein" target="_blank">read more</a></p> https://greenmedinfo.com/article/cerebral-ischemia-was-protected-oleuropein#comments Brain Ischemia Middle Cerebral Artery Occlusion (MCAO) Oleuropein Anti-Apoptotic Neuroprotective Agents Animal Study Sat, 04 May 2019 01:23:29 +0000 greenmedinfo 186891 at https://greenmedinfo.com Crocin, a constituent of Saffron, can significantly reduce infarcted areas caused by occlusion of the middle cerebral artery (MCA) in mice. https://greenmedinfo.com/article/crocin-constituent-saffron-can-significantly-reduce-infarcted-areas-caused-occ PMID:  Biochim Biophys Acta. 2007 Apr;1770(4):578-84. Epub 2006 Dec 5. PMID: 17215084 Abstract Title:  Protective effects of carotenoids from saffron on neuronal injury in vitro and in vivo. Abstract:  Crocus sativus L. (saffron) has been used as a spice for flavoring and coloring food preparations, and in Chinese traditional medicine as an anodyne or tranquilizer. Our previous study demonstrated that crocin, a carotenoid pigment of saffron, can suppress the serum deprivation-induced death of PC12 cells by increasing glutathione (GSH) synthesis and thus inhibiting neutral sphingomyelinase (nSMase) activity and ceramide formation. The carotenoid pigments of saffron consist of crocetin di-(beta-d-glucosyl)-ester [dicrocin], crocetin-(beta-d-gentiobiosyl)-(beta-d-glucosyl)-ester [tricrocin] and crocetin-di-(beta-d-gentiobiosyl)-ester [crocin]. Saffron also contains picrocrocin, the substance causing saffron&#039;s bitter taste. In this study, to confirm whether neuroprotective effects of saffron are caused solely by crocin, we examined the antioxidant and GSH-synthetic activities of these crocins in PC12 cells under serum-free and hypoxic conditions. Measurements of cell viability, peroxidized membrane lipids and caspase-3 activity showed that the rank order of the neuroprotective potency at a concentration of 10 muM was crocin&gt;tricrocin&gt;dicrocin and picrocrocin (the latter two crocins had a little or no potency). In addition, we show that among these saffron&#039;s constituents, crocin most effectively promotes mRNA expression of gamma-glutamylcysteinyl synthase (gamma-GCS), which contributes to GSH synthesis as the rate-limiting enzyme, and that the carotenoid can significantly reduce infarcted areas caused by occlusion of the middle cerebral artery (MCA) in mice. https://greenmedinfo.com/article/crocin-constituent-saffron-can-significantly-reduce-infarcted-areas-caused-occ#comments Carotenoids Crocin Middle Cerebral Artery Occlusion (MCAO) Saffron Antioxidants Neuroprotective Agents Animal Study Thu, 14 Jan 2010 03:27:23 +0000 greenmedinfo 49069 at https://greenmedinfo.com Curcumin (from Turmeric) has a protective effect against Middle Cerebral Artery Occlusion (MCAO) https://greenmedinfo.com/article/curcumin-turmeric-has-protective-effect-against-middle-cerebral-artery-occlusi PMID:  Neurochem Res. 2008 Jun;33(6):1036-43. Epub 2008 Jan 18. PMID: 18204970 Abstract Title:  Anti-ischemic effect of curcumin in rat brain. Abstract:  Turmeric has been in use since ancient times as a condiment and due to its medicinal properties. Curcumin, the yellow colouring principle in turmeric, is polyphenolic and major active constituent. Besides anti-inflammatory, thrombolytic and anticarcinogenic activities, curcumin also possesses strong antioxidant property. In view of the novel combination of properties, neuroprotective efficacy of curcumin was studied in rat middle cerebral artery occlusion (MCAO) model. Rats were subjected to 2 h of focal ischemia followed by 72 h of reperfusion. They were pre-treated with curcumin (100 mg/kg, po) for 5 days prior to MCAO and for another 3 days after MCAO. The parameters studied were behavioural, biochemical and histological. Treatment with curcumin could significantly improve neurobehavioral performance compared to untreated ischemic rats as judged by its effect on rota-rod performance and grid walking. A significant inhibition in lipid peroxidation and an increase in superoxide dismutase (SOD) activity in corpus striatum and cerebral cortex was observed following treatment with curcumin in MCAO rats as compared to MCAO group. Intracellular calcium levels were decreased following treatment with curcumin in MCAO rats. Histologically, a reduction in the infarct area from 33% to 24% was observed in MCAO rats treated with curcumin. The study demonstrates the protective efficacy of curcumin in rat MCAO model. https://greenmedinfo.com/article/curcumin-turmeric-has-protective-effect-against-middle-cerebral-artery-occlusi#comments Brain Ischemia Cerebral Ischemia Cerebral Stroke Curcumin Middle Cerebral Artery Occlusion (MCAO) Stroke: Attenuation/Recovery Stroke: Prevention Animal Study Mon, 20 Apr 2009 06:08:10 +0000 greenmedinfo 41300 at https://greenmedinfo.com