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Objective To explore the effects of morroniside on the expression of CD34 in ipsilateral cortex of rats after focal cerebral isch-emia-reperfusion. Methods 45 male Sprague-Dawley rats were divided into sham group (n=9), ischemia group (n=9), and morroniside groups (low, medium and high dosage groups, n=9). The middle cerebral artery were occluded for 30 minutes, and reperfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg, 270 mg/kg after operation. The expression of CD34 in the isch-emic ipsilateral cortex were detected with immunohistochemistry (n=6) and Western blotting (n=3) 7 days after operation. Results The ex-pression of CD34 increased in the ischemia group compared with the sham group, and further increased in the morroniside groups of high dos-age compared with the ischemia group (F>14.865, P<0.001). Conclusion Morroniside could increase the expression of CD34 in the ischemic ipsilateral cortex after ischemia-reperfusion in rats, which may promote the angiogenesis and neurogenesis after ischemia.
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Objective To explore the effects of morroniside on the expression of Angiopoietin-1 (Ang-1) and Tie-2 in a rat after focal ce-rebral ischemia-reperfusion. Methods 20 male Sprague-Dawley rats were randomly divided into sham group (n=4), ischemia group (n=4), and morroniside groups (low, medium and high dosage groups, n=4). The middle cerebral artery were occluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg after operation. The expression of Ang-1 and Tie-2 in the ischemic ipsilateral cortex were detected with Western blotting analysis 7 days after operation. Results The expres-sion of Ang-1 and Tie-2 increased in the ischemia group compared with the sham group (P<0.01), and both of them further increased in the morroniside groups of high dosage compared with the ischemia group (P<0.01), and the expression of Tie-2 also increased in the morroni-side groups of medium dosage (P<0.001). Conclusion Morroniside could increase the expression of Ang-1 and Tie-2 in the ischemic ipsilat-eral cortex after ischemia-reperfusion in rats, suggesting promoting the angiogenesis after ischemia.
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Objective To study the effects of morroniside on the expression of Wnt signaling-related transcription factors neurogenin 2 (Ngn2), Pax6 and Tbr2 in the ischemic ipsilateral cortex 7 days after cerebral ischemia-reperfusion in rats. Methods 15 male Sprague-Dawley rats were randomly divided into sham group (n=3), ischemia group (n=3), and morroniside groups (low, medium and high dosage groups, n=3). The middle cerebral artery were occluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg 3 hours after operation. The expression of Ngn2, Pax6 and Tbr2 in the ischemic ipsilateral cortex were detected with Western blotting analysis 7 days after operation. Results The expression of Ngn2 increased in the ischemia group compared with the sham group (P<0.05), and it further increased the morroniside groups of medium and high dosage compared with the ischemia group (P<0.01). There was no significant difference between the ischemia group and sham group in the expression of Pax6, while it increased the morroniside groups of medium and high dosage compared with the ischemia group (P<0.01). There was no significant difference among all the groups in the expression of Tbr2. Conclusion Morroniside could increase the expression of Ngn2 and Pax6 in the ischemic ipsilateral cortex 7 days after ischemia-reperfusion in rats, suggesting promoting the neurogenesis after ischemia.
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Objective To study the effects of morroniside on the expression of matrix metalloproteinase (MMP)-2 and MMP-9 in the peri-infarct cortex 3 days after cerebral ischemia-reperfusion. Methods 15 male Sprague-Dawley rats were randomly divided into sham group (n=3), ischemia group (n=3), and morroniside groups (low, medium and high dosage groups, n=3). The middle cerebral artery were oc-cluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg 3 hours after operation. The expression of MMP-2 and MMP-9 in peri-infarct cortex were detected with immunohistochemistry staining 3 days after operation. Results The expression of MMP-2 and MMP-9 increased in the ischemia group compared with the sham group (P<0.01), and it decreased in all the morroniside groups compared with the ischemia group (P<0.01). Conclusion Morroniside could decrease the expression of MMP-2 and MMP-9 in the peri-infarct cortex 3 days after ischemia, suggesting protecting the function of blood-brain barri-er from ischemia.
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@#Objective To explore the effects of morroniside on the expression of Angiopoietin-1 (Ang-1) and Tie-2 in a rat after focal cerebral ischemia-reperfusion. Methods 20 male Sprague-Dawley rats were randomly divided into sham group (n=4), ischemia group (n=4), and morroniside groups (low, medium and high dosage groups, n=4). The middle cerebral artery were occluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg after operation. The expression of Ang-1 and Tie-2 in the ischemic ipsilateral cortex were detected with Western blotting analysis 7 days after operation. Results The expression of Ang-1 and Tie-2 increased in the ischemia group compared with the sham group (P<0.01), and both of them further increased in the morroniside groups of high dosage compared with the ischemia group (P<0.01), and the expression of Tie-2 also increased in the morroniside groups of medium dosage (P<0.001). Conclusion Morroniside could increase the expression of Ang-1 and Tie-2 in the ischemic ipsilateral cortex after ischemia-reperfusion in rats, suggesting promoting the angiogenesis after ischemia.
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@#Objective To study the effects of morroniside on the expression of matrix metalloproteinase (MMP) -2 and MMP-9 in the peri- infarct cortex 3 days after cerebral ischemia- reperfusion. Methods 15 male Sprague-Dawley rats were randomly divided into sham group (n=3), ischemia group (n=3), and morroniside groups (low, medium and high dosage groups, n=3). The middle cerebral artery were occluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg 3 hours after operation. The expression of MMP-2 and MMP-9 in peri-infarct cortex were detected with immunohistochemistry staining 3 days after operation. Results The expression of MMP-2 and MMP-9 increased in the ischemia group compared with the sham group (P<0.01), and it decreased in all the morroniside groups compared with the ischemia group (P<0.01). Conclusion Morroniside could decrease the expression of MMP-2 and MMP-9 in the peri-infarct cortex 3 days after ischemia, suggesting protecting the function of blood-brain barrier from ischemia.
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@#Objective To study the effects of morroniside on the expression of Wnt signaling-related transcription factors neurogenin 2 (Ngn2), Pax6 and Tbr2 in the ischemic ipsilateral cortex 7 days after cerebral ischemia-reperfusion in rats. Methods 15 male Sprague-Dawley rats were randomly divided into sham group (n=3), ischemia group (n=3), and morroniside groups (low, medium and high dosage groups, n=3). The middle cerebral artery were occluded for 30 min, and re-perfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg and 270 mg/kg 3 hours after operation. The expression of Ngn2, Pax6 and Tbr2 in the ischemic ipsilateral cortex were detected with Western blotting analysis 7 days after operation. Results The expression of Ngn2 increased in the ischemia group compared with the sham group (P<0.05), and it further increased the morroniside groups of medium and high dosage compared with the ischemia group (P<0.01). There was no significant difference between the ischemia group and sham group in the expression of Pax6, while it increased the morroniside groups of medium and high dosage compared with the ischemia group (P<0.01). There was no significant difference among all the groups in the expression of Tbr2. Conclusion Morroniside could increase the expression of Ngn2 and Pax6 in the ischemic ipsilateral cortex 7 days after ischemia-reperfusion in rats, suggesting promoting the neurogenesis after ischemia.
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Tissues and organs generate angiogenesis under the stimulation of angiogenic factors in physiological or pathological conditions.Multiple signal pathways including VEGF, Notch, Wnt/β-catenin, Ang1(2)/tie2 and PIK-Akt etc.have effects on various stages of angiogenesis.VEGF exerts irreplaceable effects on the whole process of angiogenesis through multiple signal pathways.Over the past few years, new progress has been made in the researches of mechanisms regulating angiogenesis through VEGF-related signal pathways both at home and abroad.These findings provide us new theoretical basis for clarification of the pathogenesis of many diseases and clinical drug development.In this article we will summarize the recent research progress in this field, hoping to provide new possibilities for the treatment of angiogenesis-related diseases.
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@#Objective To investigate the effects of morroniside on the expression of vascular endothelial growth factor (VEGF) and fi-broblast growth factor-2 (FGF-2) in rat cortex after focal cerebral ischemia-reperfusion. Methods 30 male Sprague-Dawley rats were ran-domly divided into sham group, model group, morroniside-low group (30 mg/kg), morroniside-middle group (90 mg/kg) and morroni-side-high group (270 mg/kg). Middle cerebral arteries of rats were occluded for 30 minutes with Longa's method and re-perfused. The ex-pression of VEGF and FGF-2 in the ischemic ipsilateral cortex was detected with Western blotting 7 days after reperfusion. Results The ex-pression of both VEGF and FGF-2 increased in the ischemic ipsilateral cortexin in all the ischemic groups compared with the sham group (P<0.05). The expression of VEGF further increased in a dose-dependent manner in all the morroniside groups compared with that of model group (P<0.05), and the expression of FGF-2 increased in the morroniside-high group (P<0.001). Conclusion Morroniside could increase the expression of VEGF and FGF-2 after ischemia-reperfusion, which might promote angiogenesis.
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@#Objective To investigate the effect of morroniside on hematocrit percentage in a rat model of focal cerebral ischemia/reperfusion.Methods After the modified model induced with occlusion of middle cerebral artery (MCAO) with suture embolus, morroniside was administered intragastrically at the dose of 30 mg/kg (n=8), 90 mg/kg (n=8), and 270 mg/kg (n=8) once a day for 7 d. Acetyl salicylic acid (ASA) was used as positive drug (n=8). Hematocrit percentage was measured with automatic blood tester. Results Compared with the sham group, hematocrit percentage of the model group significantly increased (P<0.001), but increased less in those treated with morroniside and ASA (P<0.05). Conclusion Morroniside could inhibit the increase of hematocrit percentage in MCAO rats.
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@#Objective To observe the expression of phosphorylated EphrinB2 in brain after focal cerebral ischemia/reperfusion in rats.Methods 24 male Sprague-Dawley rats were randomly divided into sham group (n=12) and model group (n=12). The model group was modeled as middle cerebral artery occlusion and reperfusion with nylon monofilament suture, and then was assessed with Longa's score. The expression of phosphorylated EphrinB2 in cerebral cortex was detected with immunohistochemistry and Western blotting. Results The expression of phosphorylated EphrinB2 and the number of positive cells were significantly higher in the sham group than in the control group (P<0.05). It existed in the vascular endothelium in cerebral cortex. Conclusion EphrinB2 signaling pathway is activated in ischemic stroke.
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@#Parkinson's disease (PD) is one of the most prevalent neurodegenerative movement disorder in human being, characterized by progressive degeneration and lost of dopamine (DA)-producing neurons in the substantia nigra pars compacta (SNpc),causing low level of DA in the nigrostriatal pathway, eventually leading to motor dysfunctions including tremor, rigidity, bradykinesia,and postural instability.The pathology of PD is complex and the etiology remains poorly understood. In recent years,inflammation has been suggested to be involved in the occurrence and development of PD, by activation of microglia and overexpression of the inflammatory factors. And anti-inflammatory drugs has been developed to delay or prevent the progressive course of PD, becoming a new hotspot in treatment of PD. In this review, the latest progresses on the inflammatory mechanisms and anti-inflammatory treatments of PD was introduced.
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@#Atherosclerosis is the common basic pathophysiology progresses of acute cardiovascular and cerebrovascular diseases. Atherosclerotic plaque rupture and consequently thrombosis are the major cause of mobility and mortality in atherosclerosis, and treatment aimed at stabilizing vulnerable plaques is of great clinical importance. However, an ideal drug for stabilizing vulnerable plaques is still lacking. Although Statins are considered as the most potent drugs for stabilizing plaques, their side effects are serious. Traditional Chinese medicine have multi-targets and less side effect, it might be the potential candidate for atherosclerosis treatment. This article reviewed the latest progresses on the stabilizing vulnerable plaques treatments.
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@#Neural stem cells (NSCs), which will proliferate and differentiate into neurons and glial cells under certain conditions, involved in the repair of neurological function. This process is called neurogenesis. Focal cerebral ischemia-reperfusion injury is one of the most common diseases, which can induce the neurological functional deficits. It is significant to study the response and regulation of NSCs after focal cerebral ischemia-reperfusion injury. In this article, we reviewed the characteristics, molecular mechanisms, putative endogenous mediators and exogenous stimulators of neurogenesis in adult brain following ischemic injury, and response and regulation of drug in ischemic injury following neurogenesis.
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@#ObjectiveTo investigate the effects of morroniside on super oxide dismutase (SOD) and neurons in rats cortex with focal cerebral ischemia/reperfusion. MethodsThe animal model was induced by middle cerebral artery occlusion with suture embolus, cerebral ischemia 30 min and reperfusion 3 d or 7 d. Vitamin E for the positive control. The content of SOD was detected with spectrophotometry and the nerve cells was observed with immunohistochemistry. ResultsCompared with model group, morroniside （270 mg/kg）increased the activity of SOD and the number of neurons （30 mg/kg, 90 mg/kg, 270 mg/kg） significantly. ConclusionMorroniside may have neuroprotective effect and increasing the activity of SOD in rats cortex.
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@#Cerebral ischemia-reperfusion results in damage on neuron, leading to genes and proteins related to apoptosis activation. At the same time, generous cytokines released after cerebral ischemia-reperfusion can induce the apoptosis of the neuron. Many current studies have showed that the major damage mechanisms on apoptosis of the neuron are mitochondrion impairment, calcium overload, increased levels of oxygen radicals and so on. The advance research on the mechanism contributes to explore new neuroprotective drugs, and further identify the target and therapeutic effect of drug treatment.
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@#ObjectiveTo investigate the effects of morroniside on IL-1β in rat cortex with focal cerebral ischemia/reperfusion.MethodsThe animal model was induced by occlusion of middle cerebral artery with suture embolus, ischemia for 30 min, and reperfusion for 72 h in rats. The content of IL-1β was detected with enzyme linked immunosorbent assay(ELISA).ResultsCompared with sham group, the content of IL-1β increased obviously in model rat. Compared with model group, morroniside(30 mg/kg, 90 mg/kg, 270 mg/kg) and colchicine (0.06 mg/kg) decreased the content of IL-1β significantly (P<0.001).ConclusionMorroniside may protect the cortex from inflammatory factor IL-1β.
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@#ObjectiveTo observe the effects of Jintong capsule on model rats of Tourette syndrome (TS) and explore its probable pharmacological mechanisms.MethodsSD rats were randomly divided into six groups: blank control, TS model, haloperidol and three Jintong capsule treated groups. Model rats were copied by intraperitoneal injection of iminodipropionitrile (IDPN). The stereotyped behaviors of model rats were recorded. Open field test was used to detect ability of space recognition of rats, high performance liquid chromatography was used to detect content of monoamines, and flow cytometry was used to detect the ratio of T lymphocyte.ResultsJintong capsule can ameliorate the stereotyped behaviors of model rats, decrease content of dopamine in striatum and increase the ratio of CD4/CD8.ConclusionJintong capsule can improve behaviors of model rats. The potential mechanism of Jintong capsule maybe: it can affect the dopaminergic system of model rats, and Jintong can enhance the immune system of model rats.
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@#Objective To investigate the effects of morroniside on activation of caspase-3 in rats with focal cerebral ischemia/reperfusion. MethodsThe model was induced with occlusion of middle cerebral artery with suture embolus, ischemia for 30 min, and reperfusion for 72 h in rats. Vitamin E used for the positive control. The activity of caspase-3 was detected with spectrophotometry. ResultsCompared with sham group, the caspase-3 activity increased obviously in model rat. Compared with model group, Morroniside (30 mg/kg,90 mg/kg,270 mg/kg) decreased the activation of caspase-3 remarkably, which was dose-dependent (P<0.05). ConclusionMorroniside may reduce apoptosis by decreasing the activation of caspase-3 in rats.
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@#Objective To investigate the effects of morroniside on glutathione (GSH) and Caspase-3 in rats with focal cerebral ischemia/reperfusion. Methods The animal model was induced by middle cerebral artery occlusion with suture embolus with 30 min for cerebral ischemia and 7 d for reperfusion. The content of GSH was detected with spectrophotometry and Caspase-3 expression was observed by Western blot.Results Compared with model group, the GSH increased and Caspase-3 expression reduced significantly at 270 mg/kg of morroniside.Conclusion Morroniside may have neuroprotective effect by increasing GSH in rats cortex and reduce the apoptosis in focal cerebral ischemia/reperfusion injury.