Hua-Pin Huang

Fujian Medical University, Min-hou, Fujian, China

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Publications (14)19.18 Total impact

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    ABSTRACT: We analyzed the dynamic concentration change of serotonin (5-HT) and its main metabolite 5-hydroxyindoleacetic acid (5-HIAA) within the epileptic hippocampus in rats. Seizure was induced by systemic injection of pilocarpine (320mg/kg, i.p.). Using electroencephalography (EEG) recordings, we found that primary seizure discharge was induced 30min after pilocarpine administration and that recurrent discharge peaked 14 d after the onset of status epilepticus (SE). The extracellular fluid in the hippocampus was sampled by microdialysis from conscious animals at various time points before and after SE. The concentrations of 5-HT and 5-HIAA in the samples were measured by high-performance liquid chromatography and electrochemical detection (HPLC-ECD). Interestingly, 5-HT levels in the hippocampus were dramatically increased within the 30min following SE. This reversed to basal level by 4 d after SE and continued to drop to 48% at 7 d and 28% of basal level 14 d after SE. Accordingly, a marked increase of 5-HIAA in the hippocampus appeared at 2 d after SE, then gradually declined to levels below baseline. To identify serotonergic neurons in the raphe nuclei (a major source of 5-HT release in the brain), brain sections were immunostained for tryptophan hydroxylase (TPH). The number of TPH positive neurons and the intensity of TPH staining significantly decreased at 28 days after SE. These data suggest that pilocarpine induces depletion of 5-HT in the hippocampus and significantly compromise serotonergic neurons in the raphe nuclei. The loss of serotonergic function may play a significant role in the pathophysiology of epilepsy.
    Neuroscience Letters 12/2012; · 2.03 Impact Factor
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    ABSTRACT: To investigate the relationship between serotonin (5-HT) and epilepsy and the mechanism of learning-memory in pilocarpine (PILO)-induced epileptic rats after 5,7-dihydroxytryptamine (5,7-DHT) microinjection in median raphe nucleus. Adult S D rats were randomly divided into 3 groups: PILO group, PILO+ 5,7-DHT group, vehicle control group; PILO group was divided into two groups by status epilepticus (SE): PILO + SE group and PILO - SE group. The rats' seizures and cortex electroencephalography (EEG) were observed by vedio EEG. The rats' spatial learning-memory was evaluated by Morris water maze. Finally, serotonergic neuron in raphe nuclei was observed by immunohistochemisty. After treatment of 5,7-DHT (PILO + 5,7-DHT group), the success rate, the mortality and the frequency of chronic spontaneous seizures in pilocarpine-induced epilepsy model were all improved. Compared with the control group, the number of serotonergic neuron in raphe nuclei was decreasein PILO + SE group (P < 0.05). Moreover, it's extremely decrease in PILO + 5,7-DHT group (P < 0.01). Compared with control group, the mean escape latency was prolonged, the times of crossing target was decreased and the retention time in target zone was shortened in PILO + SE group (P < 0.05), but there was no significant difference between PILO + SE group and PILO + 5,7-DHT group. Depletion of serotonin may facility the rats' epileptic seizures, but we could not interpret which may cause epileptic rats' cognitive deficit.
    Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 05/2012; 28(3):210-3.
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    ABSTRACT: To investigate the effect of ginsenoside Rb1 on voltage-gated calcium currents in cultured rat hippocampal neurons and the modulatory mechanism. Cultured hippocampal neurons were prepared from Sprague Dawley rat embryos. Whole-cell configuration of the patch-clamp technique was used to record the voltage-gated calcium currents (VGCCs) from the hippocampal neurons,and the effect of Rb1 was examined. Rb1 (2-100 μmol/L) inhibited VGCCs in a concentration-dependent manner, and the current was mostly recovered upon wash-out. The specific L-type Ca(2+) channel inhibitor nifedipine (10 μmol/L) occluded Rb1-induced inhibition on VGCCs. Neither the selective N-type Ca(2+) channel blocker ω-conotoxin-GVIA (1 μmol/L), nor the selective P/Q-type Ca(2+) channel blocker ω-agatoxin IVA (30 nmol/L) diminished Rb1-sensitive VGCCs. Rb1 induced a leftward shift of the steady-state inactivation curve of I(Ca) to a negative potential without affecting its activation kinetics or reversal potential in the I-V curve. The inhibitory effect of Rb1 was neither abolished by the adenylyl cyclase activator forskolin (10 μmol/L), nor by the PKA inhibitor H-89 (10 μmol/L). Ginsenoside Rb1 selectively inhibits the activity of L-type voltage-gated calcium channels, without affecting the N-type or P/Q-type Ca(2+) channels in hippocampal neurons. cAMP-PKA signaling pathway is not involved in this effect.
    Acta Pharmacologica Sinica 03/2012; 33(4):438-44. · 2.35 Impact Factor
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    ABSTRACT: To explore the mechanisms of adipose-derived stem cells (ADSCs) transplanting induced angiogenesis in rat brain after focal cerebral ischemia. 108 male adult Sprague-Dawley rats were randomly assigned into 4 groups: sham-operated group, middle cerebral artery occlusion (MCAO) group, vehicle group and MCAO+ADSCs-treated group. Rat's focal cerebral ischemia model was established by right middle cerebral artery occlusion (MCAO) with modified Longa's method. ADSCs were pre-labeled by CFSE before the transplantation into the rat brain. At 1 d after MCAO, 30 μL cell suspension which contained 1×10(6); ADSCs was injected into the lateral ventricle of MCAO+ADSCs-treated rats, and the same dose of PBS was given to the rats of vehicle group as control. At 4 d, 7 d and 14 d after MCAO, rats were decapitated to detect the TGF-β1 expression in the infarct area. The expression of TGF-β1 in brain tissues in MCAO+ADSCs-treated group was significantly higher than MCAO group and vehicle group at 4 d, 7 d and 14 d after MCAO, respectively. After transplantation into MCAO rats, ADSCs could survive and express TGF-β1 in the ischemic brain. These data suggest that ADSCs transplantation can promote revascularization in cerebral ischemic rats, partly by promoting TGF-β1 expression in the brain.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 08/2011; 27(8):872-5.
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    ABSTRACT: Reactive microglia are associated with β-amyloid (Aβ) deposit and clearance in Alzhiemer's Disease (AD). Paradoxically, entocranial resident microglia fail to trigger an effective phagocytic response to clear Aβ deposits although they mainly exist in an "activated" state. Oligomeric Aβ (oAβ), a recent target in the pathogenesis of AD, can induce more potent neurotoxicity when compared with fibrillar Aβ (fAβ). However, the role of the different Aβ forms in microglial phagocytosis, induction of inflammation and oxidation, and subsequent regulation of phagocytic receptor system, remain unclear. We demonstrated that Aβ(1-42) fibrils, not Aβ(1-42) oligomers, increased the microglial phagocytosis. Intriguingly, the pretreatment of microglia with oAβ(1-42) not only attenuated fAβ(1-42)-triggered classical phagocytic response to fluorescent microspheres but also significantly inhibited phagocytosis of fluorescent labeled fAβ(1-42). Compared with the fAβ(1-42) treatment, the oAβ(1-42) treatment resulted in a rapid and transient increase in interleukin 1β (IL-1β) level and produced higher levels of tumor necrosis factor-α (TNF-α), nitric oxide (NO), prostaglandin E2 (PGE2) and intracellular superoxide anion (SOA). The further results demonstrated that microglial phagocytosis was negatively correlated with inflammatory mediators in this process and that the capacity of phagocytosis in fAβ(1-42)-induced microglia was decreased by IL-1β, lippolysaccharide (LPS) and tert-butyl hydroperoxide (t-BHP). The decreased phagocytosis could be relieved by pyrrolidone dithiocarbamate (PDTC), a nuclear factor-κB (NF-κB) inhibitor, and N-acetyl-L-cysteine (NAC), a free radical scavenger. These results suggest that the oAβ-impaired phagocytosis is mediated through inflammation and oxidative stress-mediated mechanism in microglial cells. Furthermore, oAβ(1-42) stimulation reduced the mRNA expression of CD36, integrin β1 (Itgb1), and Ig receptor FcγRIII, and significantly increased that of formyl peptide receptor 2 (FPR2) and scavenger receptor class B1 (SRB1), compared with the basal level. Interestingly, the pre-stimulation with oAβ(1-42) or the inflammatory and oxidative milieu (IL-1β, LPS or t-BHP) significantly downregulated the fAβ(1-42)-induced mRNA over-expression of CD36, CD47 and Itgb1 receptors in microglial cells. These results imply that Aβ oligomers induce a potent inflammatory response and subsequently disturb microglial phagocytosis and clearance of Aβ fibrils, thereby contributing to an initial neurodegenerative characteristic of AD. Antiinflammatory and antioxidative therapies may indeed prove beneficial to delay the progression of AD.
    Molecular Neurodegeneration 06/2011; 6:45. · 4.01 Impact Factor
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    ABSTRACT: Spinal meningoceles are uncommon entities, mostly associated with neurofibromatosis type 1 (NF-1). Their intrusion into the thoracic cavity, which compresses lung tissue, is quite often mistaken as a "pleural effusion." The withdrawal of a large amount of "pleural effusion" can lead to the intracranial hypotension syndrome (IHS), herniation, or even death. A 43-year-old woman, with NF-1 and a large "pleural effusion" which compressed lung tissue, was admitted to the Thoracic Department due to the patient's shortness of breath during her physical activities. The patient complained of headache shortly after withdrawal of about 250 mL of "pleural effusion." She was diagnosed with IHS according to the typical symptoms of postural headache, low cerebrospinal fluid (CSF) pressure and magnetic resonance imaging findings of diffuse pachymeningeal gadolinium enhancement. The "pleural effusion" was examined and found to be CSF. The reported case is the first 1 in the literature in which the intrusion of the NF-1 patient's spinal meningoceles into the thoracic cavity was diagnosed as a "pleural effusion" and large CSF withdrawal led to IHS. We highlight the possibility that thoracic meningoceles can coexist with a thoracic spinal deformity and the caution that needs to be taken when cases with similar symptoms are subjected to withdrawal of fluid.
    The Neurologist 05/2011; 17(3):167-71. · 1.48 Impact Factor
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    ABSTRACT: To observe the dynamics of hippocampal release of glutamate (Glu) and gamma-aminobutyric acid (GABA) in epilepsy (TLE) after administration with high frequency stimulation (HFS). The SD were divided into four groups (n =10): (1) Control group (KB) the rats were injected intraperitoneally with saline 0.9%. (2) Kainic acid (KA) group: the rats were injected with KA. (3) Pseudo-deep brain stimulation (DBS) group: the KA-induced rats were implanted with rheophores alone. (4) DBS group: KA induced-rats with DBS in hippocampal epileptic foci. We then collected hippocampal extracellular fluid by microdialysis and the levels of Glu and GABA were measured by high-performance liquid chromatography (HPLC) and fluorescence detection. There was no difference in the baseline of Glu and GABA in the four groups. In contrast, a significant increase in the content of Glu and GABA was shown in the three periods of KA-kindled seizures. Electrical stimulation of hippocampus resulted in a decrease of hippocampal Glu contents, while there was no change in GABA contents. Additionally, HFS of hippocampus normalized the Glu/GABA ratio in the chronic period of seizures. The high frequency stimulation of epileptic foci may protect against seizures by modulating the extracellular release of hippocampal Glu.
    Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 02/2011; 27(1):88-92.
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    ABSTRACT: to explore the effects of IL-10 on the expression of interferon regulatory factor-1 (IRF-1) after anoxia-reoxygenation in vitro. brain microvascular endothelial cells (BMEC) and neutrophil (PMN) were co-cultured exposed to eight hours of anoxia followed by two hours of reoxygenation to establish anoxia-reoxygenation model in vitro. The co-cultured BMEC and PMN were randomly divided into the following groups: normal group, anoxia-reoxygenation group, 1 microg/L IL-10 treatment group, 10 microg/L IL-10 treatment group, and 30 microg/L IL-10 treatment group. The expression of IRF-1 was detected by RT-PCR and Western blot method. the expression of IRF-1 was significantly upregulated after anoxia-reoxygenation. IL-10 inhibited the expression of IRF-1 in a dose-dependent manner compared with anoxia-reoxygenation group, and the peak of inhibitive effects occurred at the dose of 30 μg/L. IL-10 can inhibit the expression of interferon regulatory factor-1 with anoxia-reoxygenation in vitro.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 10/2010; 26(10):969-72.
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    ABSTRACT: Recent research has focused on soluble oligomeric assemblies of beta-amyloid peptides (Abeta) as the proximate cause of neuroinflammation, synaptic loss, and the eventual dementia associated with Alzheimer's disease (AD). In this study, tripchlorolide (T4), an extract of Tripterygium wilfordii Hook. F (TWHF), was studied as a novel agent to suppress neuroinflammatory process in microglial cells and to protect neuronal cells against microglia-mediated oligomeric Abeta toxicity. T4 significantly attenuated oligomeric Abeta(1-42)-induced release of inflammatory productions such as tumor necrosis factor-alpha, interleukin-1beta, nitric oxide (NO), and prostaglandin E2. It also downregulated the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in microglial cells. Further molecular mechanism study demonstrated that T4 inhibited the nuclear translocation of nuclear factor-kappaB (NF-kappaB) without affecting I-kappaBalpha phosphorylation. It repressed Abeta-induced JNK phosphorylation but not ERK or p38 MAPK. The inhibition of NF-kappaB and JNK by T4 is correlated with the suppression of inflammatory mediators in Abeta-stimulated microglial cells. These results suggest that T4 protects neuronal cells by blocking inflammatory responses of microglial cells to oligomeric Abeta(1-42) and that T4 acts on the signaling of NF-kappaB and JNK, which are involved in the modulation of inflammatory response. Therefore, T4 may be an effective agent in modulating neuroinflammatory process in AD.
    Glia 02/2009; 57(11):1227-38. · 5.07 Impact Factor
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    ABSTRACT: To investigate the inhibiting effects of interleukin-10 (IL-10) on the expression of E-selectin and L-selectin in cerebral ischemia-reperfusions. Seventy-two adult male Sprague-Dawley rats were randomly divided into 4 equal groups, cerebral ischemia-reperfusion (I/R) group undergoing middle cerebral artery occlusion with Longa's thread method, IL-10 group undergoing lateral ventricle injection of IL-10 after the establishment of I/R model, Vehicle group undergoing lateral ventricle injection of normal saline after the establishment of I/R model, and sham operation (Sham) group. Twenty-four hours later the rats were killed with their brains taken out. Immunohistochemistry, RT-PCR and Western blotting were used to detect the mRNA and protein expression of E-selectin and L-selectin. The E-selectin and L-selectin expression levels of the I/R group were significantly up-regulated compared with the Sham group (both P < 0.05). The numbers of E-selectin and L-selectin positive vessels of the IL-10 group were 18.8 +/- 1.9/10 HP fields and 15.8 + 2.4/10 HP fields respectively, both significantly less than those of the vehicle group (24.7 +/- 2.4/10 HP fields and 20.9 + 3.3/10 HP fields respectively, both P < 0.05). The E-selectin and L-selectin gene mRNA expression levels of the IL-10 group were (0.431 +/- 0.029) and (0.318 +/- 0.048) respectively, both significantly lower than those of the Vehicle group [(0.497 +/- 0.019) and (0.433 +/- 0.087) respectively, both P < 0.05]. The E-selectin and L-selectin protein expression levels of the IL-10 group were (0.349 +/- 0.037) and (0.296 +/- 0.035) respectively, both significantly lower than those of the Vehicle group [(0.421 +/- 0.043,) and (0.348 +/- 0.044) respectively, both P < 0.05]. IL-10 suppresses the expression of E-selectin and L-selectin in cerebral ischemia-reperfusion.
    Zhonghua yi xue za zhi 01/2009; 89(1):59-62.
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    ABSTRACT: A large body of evidence has suggested a strong association between neuroinflammation and the pathogenesis of many neurodegenerative diseases. Therefore, it is a good target for therapeutic treatment. So far, studies have proven anti-inflammatory herbal medicine and its constituents to be effective in slowing down the neurodegenerative process. The present study tested tripchlorolide, an extract of Tripterygium wilfordii Hook F (TWHF), as a novel agent to suppress inflammatory process in microglia. It showed this novel agent to be cytotoxic at a dose of 20-40 nM to primary microglia and BV-2 microglial cells but not to primary cortical neurons and Neuro-2A cells in vitro. Moreover, tripchlorolide protected primary cortical neurons and Neuro-2A cells from neuroinflammatory toxicity induced by the conditioned media from lipopolysaccharide (LPS)-stimulated microglia, which resulted in a significant decrease in their cell survival. The changes of the inflammatory mediators in this process were further investigated. In the LPS-stimulated microglia, the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), nitric oxide (NO), prostaglandin E(2) (PGE(2)), and intracellular superoxide anion (SOA) was markedly attenuated by tripchlorolide at a dose of 1.25-10 nM in a dose-dependent manner. Furthermore, the production of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was also significantly inhibited by tripchlorolide in both mRNA and protein levels. These results suggest that tripchlorolide can protect neuronal cells via a mechanism involving inhibition of inflammatory responses of microglia to pathological stimulations. Therefore, it is potentially a highly effective therapeutic agent in treating neuroninflammatory diseases.
    Biochemical pharmacology 09/2008; 76(3):362-72. · 4.25 Impact Factor
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    ABSTRACT: To explore the relationship between evoked potentials (EPs) and chronic anoxic brain damage by chronic intermittent hypoxia (CIH), and provide theory evidence for diagnosis and treatment of anoxic encephalopathy. BAEP and SLSEP were recorded in rat model with CIH (hypoxia group) and rat with normoxia (normal group). Morris water maze was used to observe learning and memory ability. Immunohistochemical method was used to investigate the expression levels of caspase-3 in brain tissue. The peak latency (PL) of wave I, III, V and the interpeak latency (IPL) of wave III - V, I - V in BAEP in hypoxia group were much longer than that of in normal group (P < 0.05). The PL of wave N1, P1 of SEP in hypoxia group were much longer than that of in normal group (P < 0.05). In the water mase test, the escape latency (EL) of hypoxia group was much longer than normal group (P < 0.01). The number of caspase-3 positive cells in hypoxia group was much larger than that of in normal group (P < 0.05). There was a positive correlation among BAEP, SLSEP, the number of caspase-3 positive neuron and EL of water mase. The alteration of BAEP and SLSEP has an apparent correlation with chronic anoxic brain damage. This provides theory evidence for diagnosis and treatment of anoxic encephalopathy.
    Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 08/2008; 24(3):301-5.
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    ABSTRACT: To investigate the effects of bone marrow-derived mesenchymal stem cells (BMSC) transplantation on the recovery of neurological functions and the expression of synaptophysin in focal cerebral infarction in rats. 72 male adult Sprague-Dawley rats were randomly divided into 4 groups (18 in each group): shamoperated group, middle cerebral artery occlusion (MCAO) roup,vehicle group and MCAO+BMSC-treated group. A permanent focal cerebral ischemia model was established using modified Longa's method. BMSC was labeled by DAPI before the transplantation. One day after right middle cerebral artery occlusion(MCAO), 1 x 10(6) cells were injected into the lateral ventricle of rats in BMSCs-treated group and the same dose of PBS was given to the rats in vehicle group. Before sacrificed and at 4 d, 7 d and 14 d after MCAO, the neurological functions were tested by balance beam, rota-rod and screen prehensile and the synaptophysin was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemical method. DAPI stained positive cells were observed around the cerebral infarcted area in the BMSC-treated group. Compared with the MCAO group and the vehicle group,the neurological functions in BMSC-treated group were better on 7 d and 14 d after MCAO (P<0.05 or P<0.01), and the synaptophysin around the cerebral infarcted area was significantly upregulated on 4 d, 7 d and 14 d after MCAO (all P<0.01). BMSC transplantation can improve the neurological functions by upregulating the expression of synaptophysin after MCAO in rats.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 01/2008; 24(1):34-7.
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    ABSTRACT: To investigate the effect of interleukin-10 on neurocyte apoptosis in cerebral ischemia in rats. 36 adult male Sprague-Dawley rats were randomly assigned into 3 groups: sham operation group, middle cerebral artery occlusion(MCAO) group and MCAO+interleukin-10 treatment group. Terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) staining was used to detect in situ cell apoptosis, immunohistochemical staining and RT-PCR were used to detect the expression of proapoptotic gene Fas, Fas ligand (FasL) and caspase-3 in peri-infarct, respectively. Cerebral ischemia significantly induced neurocyte apoptosis and upregulated the expression of Fas, FasL and caspase-3, repcetively (P<0.05). IL-10 treatment significantly inhibited neurocyte apoptosis, and suppressed the expression of proapoptotic gene FasL and caspase-3, repcetively (P<0.05), but had no obvious effect on Fas expression (P>0.05). IL-10 can suppress neurocyte apoptosis in cerebral ischemia, whose mechanisms seemed related to inhibiting the expression of proapoptotic gene FasL and caspase-3.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 06/2007; 23(6):498-500.