Hebei Institute of Cardio Cerebral Vascular Diseases

Shijiazhuang, China

Hebei Institute of Cardio Cerebral Vascular Diseases

Shijiazhuang, China
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Wang L.,Hebei Medical University | Li Z.,Hebei Medical University | Li Z.,Hebei Institute of Cardio Cerebral Vascular Diseases | Li Z.,Hebei Key Laboratory for Neurology | And 17 more authors.
Neurochemical Research | Year: 2014

Inflammatory damage plays an important role in cerebral ischemic pathogenesis and represents a new target for treatment of stroke. Shikonin has gained attention for its prominent anti-inflammatory property, but up to now little is known about shikonin treatment in acute ischemic stroke. The aim of this study was to evaluate the potential neuroprotective role of shikonin in cerebral ischemic injury, and investigate whether shikonin modulated inflammatory responses after stroke. Focal cerebral ischemia in male ICR mice was induced by transient middle cerebral artery occlusion. Shikonin (10 and 25 mg/kg) was administered by gavage once a day for 3 days before surgery and another dosage after operation. Neurological deficit, infarct volume, brain edema, blood-brain barrier (BBB) dysfunction, and inflammatory mediators were evaluated at 24 and 72 h after stroke. Compared with vehicle group, 25 mg/kg shikonin significantly improved neurological deficit, decreased infarct volume and edema both at 24 and 72 h after transient ischemic stroke, our data also showed that shikonin inhibited the pro-inflammatory mediators, including TLR4, TNF-α, NF-κB, and phosphorylation of p38MAPK in ischemic cortex. In addition, shikonin effectively alleviated brain leakage of Evans blue, up-regulated claudin-5 expression, and inhibited the over-expressed MMP-9 in ischemic brain. These results suggested that shikonin effectively protected brain against ischemic damage by regulating inflammatory responses and ameliorating BBB permeability. © 2013 Springer Science+Business Media New York.


Zhang J.,Hebei Medical University | Fu B.,Hebei Medical University | Zhang X.,Hebei Medical University | Zhang X.,Hebei Institute of Cardio Cerebral Vascular Diseases | And 8 more authors.
Brain Research | Year: 2013

Background Inflammatory damage aggravates the cerebral ischemic pathological process and may pave a new way for treatment. Bicyclol has been proved to elicit a series of biologic effects through its anti-inflammatory property in treating hepatitis and hepatic ischemic/reperfusion injury. Whether this protective effect applies to cerebral ischemic injury, we therefore investigated the potential neuroprotective role of bicyclol and the underlying mechanisms. Methods: Male Sprague-Dawley rats were randomly assigned to five groups: permanent middle cerebral artery occlusion (pMCAO), Vehicle (pMCAO+0.5% sodium carboxymethylcellulose), By-L (Vehicle+bicyclol 50 mg/kg), By-H (Vehicle+bicyclol 100 mg/kg) and Sham operated group. Bicyclol was administered intragastrically once a day for 3 days, after 1 h of bicyclol pretreatment on the third day; rat brain ischemia was induced by pMCAO. Neurological deficit, infarct volume, and brain edema were measured at 24 h after stroke. Immunohistochemistry, Western blot and real-time quantitative PCR were used to detect the expression of TLR4, TLR9, TRAF6, NF-κB and MMP-9, claudin-5. Results: Compared with pMCAO group, bicyclol significantly ameliorated neurological deficit, decreased infarct volume and edema, and down-regulated the expression of TLR4, TLR9, TRAF6, NF-κB and MMP-9 (P<0.05). Meanwhile, the expression of claudin-5 was increased (P<0.05). Conclusions: Bicyclol has neuroprotective effect on cerebral ischemia, and this protection may be through down-regulating TLR4, TLR9, TRAF6, NF-κB, MMP-9 and up-regulating claudin-5 expression. © 2013 Elsevier B.V.


Li L.,Hebei Medical University | Li L.,Hebei General Hospital | Zhang X.,Hebei Medical University | Zhang X.,Hebei Institute of Cardio Cerebral Vascular Diseases | And 6 more authors.
Brain Research | Year: 2013

Background: Oxidative and inflammatory damages have been suggested to play an important role in cerebral ischemic pathogenesis, and provide promising therapeutic strategies for stroke. Nuclear factor-erythroid 2-related factor 2 (Nrf2), a pleiotropic transcription factor, has been shown to play a key role in protecting cells against oxidative injury in cerebral ischemia. In this study, we demonstrated the hypothesis that ursolic acid (UA), a natural pentacyclic triterpenoid acid, isolated from edible plants in the Oleaceae family, a well-known anti-oxidative and anti-inflammatory reagent, protects the brain against ischemic injury by activating the Nrf2 pathway. Methods: Nrf2 -/- and wild-type (WT) mice were induced into focal cerebral ischemia by transient middle cerebral artery occlusion (MCAO), and received UA treatment immediately after MCAO. The behavioral dysfunction, infarct size, and the expression of Nrf2, HO-1 and inflammatory factors (TLR4 and NF-κB) in ischemic brain were measured at 24 h after stroke. Results: UA treatment significantly improved neurological deficit and reduced infarct size in WT mice after MCAO. Administration of UA also decreased the product of lipid peroxidation, promoted the activation of Nrf2 pathway and decreased the expression of TLR4 and NF-KB after stroke in WT mice. However, Nrf2 -/- mice demonstrated more severe neurologic deficits, infarct size and inflammatory damage after MCAO, and did not benefit from the protective effect of UA. Conclusion: The results indicated that UA protected the brain against ischemic injury in mice by anti-oxidative and anti-inflammatory effects after MCAO. Activation of the Nrf2 pathway contributes to the neuroprotective effects induced by UA in cerebral ischemia. © 2012 Elsevier B.V.


Zou Y.,Hebei Medical University | Zou Y.,Hebei Institute of Cardio Cerebral Vascular Diseases | Zou Y.,Hebei Key Laboratory for Neurology | He J.,Hebei Medical University | And 11 more authors.
Diagnostic Cytopathology | Year: 2015

Background Tuberculous meningitis is the most lethal form of tuberculosis, but current diagnostic methods are inadequate. The measurement of cerebrospinal fluid parameters can provide early information for diagnosis. The present study focus on the validity of the cut-off value of cerebrospinal fluid parameters according to the Lancet consensus of scoring system for diagnosis of tuberculous meningitis. Method A total of 100 confirmed patients were enrolled in this study. We evaluated significance of protein level (>1 g/l), chloride level (<120 mmol/l), glucose level (<2.2 mmol/l), cell counts (10-500 cells/μl, lymphocytic pleocytosis (>50%), and neutrophil predominance (>50%) in early diagnosis of tuberculous meningitis. Result The cerebrospinal fluid parameters were significantly different between the tuberculous meningitis group and the control group. The independent factors for diagnosis of tuberculous meningitis were protein level (>1 g/l), glucose level (<2.2 mmol/l), cell counts (10-500 cells/μl and neutrophil predominance >50%). Neutrophil predominance (>50%) performed the best with the area under the curve of 89.7%. The sensitivity of protein level (>1 g/l), glucose level (<2.2 mmol/l), cell counts (10-500 cells/μl) and neutrophil predominance (>50%) for diagnosis of tuberculous meningitis were 66%, 58%, 86%, and 54%, and the specificity were 84%, 98%, 32%, and 98%. There are 84% patients in tuberculous meningitis group at least having two positive parameters among the four independent parameters, while only 10% in control group. Conclusion The cerebrospinal fluid parameters can help the clinicians to make a prompt diagnosis in the early stage of the disease. Diagn. Cytopathol. 2015;43:701-704. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.


Qiao H.,Hebei Medical University | Zhang X.,Hebei Medical University | Zhang X.,Hebei Institute of Cardio Cerebral Vascular Diseases | Zhang X.,Hebei Key Laboratory for Neurology | And 9 more authors.
Brain Research | Year: 2012

Background: Inflammatory damage is known to be involved in ischemic stroke. Luteolin has been proved to elicit a series of biologic effects through its anti-inflammatory property in multiple sclerosis and rheumatoid arthritis. Whether this protective effect applies to ischemic injury in brain is still unknown, we therefore investigate the potential neuroprotective role of luteolin in ischemic stroke and the underlying mechanisms. Methods: Male Sprague-Dawley rats were subjected to pMCAO and luteolin was administered intraperitoneally immediately after surgery, then once daily thereafter. Neurological deficit, infarct volume, and brain water content were measured at 24 h and 72 h after stroke. The expression of TLR4, TLR5, and NF-κB were measured by real-time PCR, immunohistochemical staining (IHC), and Western blot. P38MAPK and extracellular signal-regulated kinase (ERK) were detected by IHC, and Western blot. Results: Compared with pMCAO group, luteolin significantly alleviated neurological deficit, decreased infarct volume and suppressed edema after ischemic stroke, which were accompanied with decreased expression of TLR4, TLR5, NF-κB and p-p38MAPK. Meanwhile, luteolin activated the expression of p-ERK1/2 (P < 0.05). Conclusions: Luteolin protected the brain from the damage caused by pMCAO, and this effect may be through downregulation of TLR4, TLR5, NF-κB, p38MAPK and upregulation of ERK expression. © 2012 Elsevier B.V. All rights reserved.


Zhu C.,Hebei Medical University | Zhu C.,Hebei Institute of Cardio Cerebral Vascular Diseases | Zhu C.,Hebei Key Laboratory for Neurology | Zhang X.,Hebei Medical University | And 9 more authors.
Neurochemical Research | Year: 2012

Inflammatory damage plays a pivotal role in cerebral ischemia and may represent a target for treatment. Pigment epithelium-derived factor (PEDF) is proven to possess neuroprotective property. But there is little known about the intrinsic PEDF after cerebral ischemia. This study evaluated the time course expression of the intrinsic PEDF and its underlying regulation mechanisms after cerebral ischemia. Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion. Telmisartan (PPARγ agonist) and GW9662 (PPARγ antagonist) were systemically administered to explore the effect on PPARγ, PEDF, NF-κB and MMP-9 expression at 24 h after cerebral ischemia by western blot and qRT-PCR. The neurological deficits, brain water content and infarct volume were measured. Compared with normal group, the expressions of PEDF and PPARγ decreased, and the expression of NF-κB and MMP-9 increased at early stage after ischemia (P<0.05). Compared with the vehicle group, the decrease of PEDF and PPARγ was significantly up-regulated and the increase of NF-κB and MMP-9 was down-regulated by telmisartan at 24 h (P<0.05). The neurological deficits, brain water content and infarct volume were dramatically alleviated by telmisartan (P<0.05). Telmisartan's effects were reversed by GW9662 co-administration (P\0.05). The expression of intrinsic PEDF was down-regulated at the early stage of cerebral ischemia. The protective effects of intrinsic PEDF by activating PPARγ pathway may be one of the strategic targets for cerebral ischemic therapies. © Springer Science+Business Media, LLC 2012.


Qiao H.,Hebei Medical University | Dong L.,Hebei Medical University | Zhang X.,Hebei Medical University | Zhang X.,Hebei Institute of Cardio Cerebral Vascular Diseases | And 10 more authors.
Neurochemical Research | Year: 2012

Luteolin recently has been proved to elicit a vanity of biological effects through its antioxidant and antiapoptosis properties. Oxidative and apoptosis damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. The aim of this study was to evaluate the neuroprotective effects of luteolin and the underlying mechanisms in cerebral ischemia. Focal cerebral ischemia was induced in adult male Sprague- Dawley rats by permanent middle cerebral artery occlusion (pMCAO). Luteolin was injected intraperitoneally at different doses of 10 or 25 mg/kg immediately after pMCAO. Experiment 1, luteolin's neuroprotective effect was analyzed. Neurological deficits, brain water content and infarct volume were evaluated at 24 and 72 h after pMCAO. SOD1, Bcl-2, and Bax expression were measured by immunohistochemistry, western blot and reverse transcription- polymerase chain reaction. Experiment 2, luteolin's anti-oxidative activities were evaluated. SOD1, CAT activities, and MDA content were measured by spectrophotometer. Experiment 3, the influence of luteolin on claudin-5 was detected. Compared with MCAO group, luteolin significantly increased the activities of SOD1, CAT, Bcl-2 and claudin-5 (P<0.05), decreased the levels of MDA and Bax (P<0.05), and alleviated the neurological deficits, infarct volume and brain water content (P<0.05). The results indicated that luteolin protected the brain from ischemic damage, and this effect may be through reduction of oxidative stress and apoptosis, and upregulation of the expressions of claudin-5.

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