Shangdong Liang

Nanchang University, Nan-ch’ang-shih, Jiangxi Sheng, China

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Publications (48)117.32 Total impact

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    ABSTRACT: Chronic inflammation plays a major role in development of type 2 diabetes mellitus (T2DM). C-reactive protein (CRP) and inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) are directly involved in the occurrence of insulin resistance. Increased extracellular ATP levels can amplify the inflammatory response in vivo via the P2X7 receptor. The present study aimed to assess the relationship between P2X7 receptor expression in human peripheral blood monocytes and plasma levels of TNF-α, IL-1β, and CRP in T2DM patients. The results showed the association of increased P2X7 receptor expression of monocytes with high serum CRP, TNF-α, and IL-1β levels. TNF-α and IL-1β levels were lowest in healthy subjects; in T2DM patients, these inflammatory markers were less abundant in individuals with normal CRP levels compared to those with high CRP contents. In contrast, IL-10 levels in T2DM patients with high CRP levels were dramatically decreased. P2X7 receptor expression in monocytes from T2DM patients with high CRP levels was significantly increased in comparison with healthy individuals and T2DM patients with normal CRP levels. These findings indicated that P2X7 receptor in peripheral blood monocytes may be involved in the pathological changes of T2DM, particularly affecting patients with high CRP levels.
    Inflammation 05/2015; DOI:10.1007/s10753-015-0189-y · 2.21 Impact Factor
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    ABSTRACT: Extracellular ATP regulates cellular function in an autocrine or paracrine manner through activating purinergic signalling. Studies have shown that purinergic receptors were expressed in mammalian ovaries and they have been proposed as an intra-ovarian regulatory mechanism. P2X7 was expressed in porcine ovarian theca cells and murine and human ovarian surface epithelium and is involved in ATP-induced apoptotic cell death. However, the role of P2X7 in corpus luteum is still unclear. The aim of this study was to investigate the role of ATP signalling in murine luteal cells and the possible mechanism(s) involved. We found that P2X7 was highly expressed in murine small luteal cells. The agonists of P2X7, ATP and BzATP, inhibited the proliferation of luteal cells. P2X7 antagonist BBG reversed the inhibition induced by ATP and BzATP. Further studies showed that ATP and BzATP inhibited the expression of cell cycle regulators cyclinD2 and cyclinE2. ATP and BzATP also inhibited the p38-mitogen-activated protein kinase (MAPK) signalling pathway. These results reveal that P2X7 receptor activation is involved in corpus luteum formation and function.
    Reproduction Fertility and Development 03/2015; DOI:10.1071/RD14381 · 2.58 Impact Factor
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    ABSTRACT: Notch signaling is an evolutionarily conserved pathway, which involves in various cell life activities. Other studies and our report showed that the Notch signaling plays very important role in follicle development in mammalian ovaries. In luteal cells, Notch ligand, delta-like ligand 4, is involved in normal luteal vasculature. In this study, murine luteal cells were cultured in vitro and treated with Notch signaling inhibitors, L-658,458 and N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycinet-butyl ester (DAPT). We found that L-658,458 and DAPT treatment decrease basal and human chorionic gonadotropin (hCG)-stimulated progesterone secretion. On the contrary, overexpression of intracellular domain of Notch3 increased basal and hCG-stimulated progesterone secretion. Further studies demonstrated that Notch signaling regulated the expression of steroidogenic acute regulatory protein and CYP11A, 2 key enzymes for progesterone synthesis. In conclusion, Notch signaling plays important role in regulating progesterone secretion in murine luteal cells. © The Author(s) 2015.
    Reproductive sciences (Thousand Oaks, Calif.) 02/2015; DOI:10.1177/1933719115572480 · 2.18 Impact Factor
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    ABSTRACT: Induction of endothelial cytotoxicity by hyperglycemia in diabetes has been widely accepted. Emodin is a natural anthraquinone in rhubarb used for treatment of diabetes, but its mechanism of action is not fully understood. This study aimed to examine the potential beneficial effects of emodin on endothelial cytotoxicity caused by high glucose milieu. Culture of human umbilical vein endothelial cells (HUVECs) with high concentrations of glucose resulted in damage to the cells, leading to decreased formazan products by 14-27%, reduced DNA contents by 12-19%, and increased hypodiploid apoptosis by 40-109%. These adverse effects of high glucose could be prevented to a large extent by co-culture with 3 μM of emodin which per se did not affect HUVECs viability. In addition, CCL5 expression of HUVECs cultured in high glucose medium was significantly elevated at both mRNA and protein levels, an effect abolished after treatment with emodin. Moreover, the enhanced adhesion of monocytes to HUVECs (2.1-2.2 fold over control) and elevated chemotaxis activities (2.3-2.4 fold over control) in HUVECs cultured in high glucose medium were completely reversed by emodin. Emodin also suppressed activation of p38 MAPK and ERK1/2 due to high glucose. Our data demonstrated that endothelial cytotoxicity occurred clearly when HUVECs were exposed to high glucose milieu and emodin was able to alleviate the impairments. The protective effects of emodin might be related to the inhibition of CCL5 expression and subsequent cell stress/inflammatory events possibly mediated by activation of MAPK signaling pathways.
    Biochemical Pharmacology 01/2015; 94(1). DOI:10.1016/j.bcp.2015.01.006 · 4.65 Impact Factor
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    ABSTRACT: Irritable bowel syndrome (IBS) and inflammatory bowel disease often display visceral hypersensitivity. Visceral nociceptors after inflammatory stimulation generate afferent nerve impulses through dorsal root ganglia (DRG) transmitting to the central nervous system. ATP and its activated-purinergic 2X7 (P2X7) receptor play an important role in the transmission of nociceptive signal. Purinergic signaling is involved in the sensory transmission of visceral pain. Moxibustion is a therapy applying ignited mugwort directly or indirectly at acupuncture points or other specific parts of the body to treat diseases. Heat-sensitive acupoints are the corresponding points extremely sensitive to moxa heat in disease conditions. In this study, we aimed to investigate the relationship between the analgesic effect of moxibustion on a heat-sensitive acupoint "Dachangshu" and the expression levels of P2X7 receptor in rat DRG after chronic inflammatory stimulation of colorectal distension. Heat-sensitive moxibustion at Dachangshu acupoint inhibited the nociceptive signal transmission by decreasing the upregulated expression levels of P2X7 mRNA and protein in DRG induced by visceral pain, and reversed the abnormal expression of glial fibrillary acidic protein (GFAP, a marker of satellite glial cells) in DRG. Consequently, abdominal withdrawal reflex (AWR) score in a visceral pain model was reduced, and the pain threshold was elevated. Therefore, heat-sensitive moxibustion at Dachangshu acupoint can produce a therapeutic effect on IBS via inhibiting the nociceptive transmission mediated by upregulated P2X7 receptor.
    Purinergic Signalling 12/2014; 11(2). DOI:10.1007/s11302-014-9439-y · 3.51 Impact Factor
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    ABSTRACT: After the myocardial ischemia, injuried myocardial tissues released large quantity of ATP, which activated P2X3 receptor in superior cervical ganglia and made the SCG postganglionic neurons excited. Excitatory of sympathetic postganglionic efferent neurons increased the blood pressure and heart rates, which aggravated the myocardial ischemic injury. Baicalin have anti-inflammatory and anti-oxidant properties. Our study showed that baicalin reduced the incremental concentration of serum CK-MB, cTn-T, epinephrine and ATP, decreased the up-regulated expression levels of P2X3 mRNA and protein in SCG after MI, and then inhibited the sympathetic excitatory activity triggered by MI injury. These results indicated that baicalin acted on P2X3 receptor were involved in the transmission of sympathetic excitation after the myocardial ischemic injury. Baicalin might decrease sympathetic activity via inhibiting P2X3 receptor in rat SCG to protect myocardium.
    Autonomic Neuroscience 12/2014; 189. DOI:10.1016/j.autneu.2014.12.001 · 1.37 Impact Factor
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    ABSTRACT: Type 2 diabetes (T2D) is characterized as hyperglycaemia caused by defects in insulin secretion, and it affects target tissues, such as skeletal muscle, liver and adipose tissue. Therefore, analyzing the changes of gene expression profiles in these tissues is important to elucidate the pathogenesis of T2D. We, therefore, measured the gene transcript alterations in liver and skeletal muscle of rat with induced T2D, to detect differentially expressed genes in liver and skeletal muscle and perform gene-annotation enrichment analysis. In the present study, skeletal muscle and liver tissue from 10 streptozotocin-induced diabetic rats and 10 control rats were analyzed using gene expression microarrays. KEGG pathways enriched by differentially expressed genes (DEGs) were identified by WebGestalt Expander and GATHER software. DEGs were validated by the method of real-time PCR and western blot. From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P<0.01) were identified in comparisons of skeletal muscle and liver, respectively. Large numbers of DEGs (200) were common in both comparisons, which was clearly more than the predicted number (131 genes, P<0.001). For further interpretation of the gene expression data, three over-representation analysis softwares (WebGestalt, Expander and GATHER) were used. All the tools detected one KEGG pathway (MAPK signaling) and two GO (gene ontology) biological processes (response to stress and cell death), with enrichment of DEGs in both tissues. In addition, PPI (protein-protein interaction) networks constructed using human homologues not only revealed the tendency of DEGs to form a highly connected module, but also suggested a "hub" role of p38-MAPK-related genes (such as MAPK14) in the pathogenesis of T2D. Our results indicated the considerably aberrant MAPK signaling in both insulin-sensitive tissues of T2D rat, and that the p38 may play a role as a common "hub" in the gene module response to hyperglycaemia. Furthermore, our research pinpoints the role of several new T2D-associated genes (such as Srebf1 and Ppargc1) in the human population.
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    ABSTRACT: Diabetic neuropathy (DNP) is the most common chronic complication of diabetes. Elevated free fatty acids (FFAs) have been recently recognized as major causes of inflammation and are relevant to the functional changes of nerve system in diabetes. Trans-resveratrol (RESV), a polyphenolic natural compound, has long been acknowledged to have anti-inflammation properties and may exert a neuroprotective effect on neuronal damage in diabetes, while the mechanisms underlying are largely unknown. Our previous study on differential PC12 cells cultured with high FFAs has shown chronic FFAs overload increased PC12 interleukin (IL)-6 release mediated by P2X7 receptor, a ligand-gated cation channel activated by extracellular adenosine triphosphate (ATP); a high FFA-induced activation of P38 mitogen-activated protein kinase (MAPK) pathway was pointed to be a potential underlying mechanism. Data from this study indicated that RESV, in a dose-dependent manner, reduced high FFA-induced IL-6 release by impeding the activation of P2X7 receptor, as shown by the results that both high FFA-elevated P2X7 receptor messenger RNA (mRNA) and protein expression as well as high FFA-evoked [Ca(2+)]i in response to 3'-O-(4-benzoyl) benzoyl-ATP (a selective P2X7 receptor agonist) were significantly attenuated. Meanwhile, high FFA-induced activation of P38 MAPK, an essential prerequisite for high FFA-activated P2X7 receptor and subsequent IL-6 release, was also dose-dependently abrogated by RESV. Furthermore, RESV may hamper the activation of P38a MAPK (one paramount P38 isoform) via forming hydrogen bonding with Thr175 residue, surrounding the two residues (Thy180 and Tyr182) essential for canonical activation of P38a MAPK. Taken together, RESV could inhibit high FFA-induced inflammatory IL-6 release mediated by P2X7 receptor through deactivation of P38 MAPK signaling pathway. All these results outline the potential mechanisms involved in the neuroprotective roles of RESV and highlight the clinical application of RESV in treatment of inflammation in relation to DNP.
    Inflammation 10/2014; 38(1). DOI:10.1007/s10753-014-0036-6 · 2.21 Impact Factor
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    ABSTRACT: Neuropathic pain is a very common complication in diabetes mellitus (DM), and treatment for it is limited. As DM is becoming a global epidemic it is important to understand and treat this problem. The mechanisms of diabetic neuropathic pain are largely obscure. Recent studies have shown that glial cells are important for a variety of neuropathic pain types, and we investigated what are the changes that satellite glial cells (SGCs) in dorsal root ganglia undergo in a DM type 1 model, induced by streptozotocin (STZ) in mice and rats. We carried out immunohistochemical studies to learn about changes in the activation marker glial fibrillary acidic protein (GFAP) in SGCs. We found that after STZ-treatment the number of neurons surrounded with GFAP-positive SGCs in dorsal root ganglia increased 4-fold in mice and 5-fold in rats. Western blotting for GFAP, which was done only on rats because of the larger size of the ganglia, showed an increase of about 2-fold in STZ-treated rats, supporting the immunohistochemical results. These results indicate for the first time that SGCs are activated in rodent models of DM1. As SGC activation appears to contribute to chronic pain, these results suggest that SGCs may participate in the generation and maintenance of diabetic neuropathic pain, and can serve as a potential therapeutic target.
    Journal of Cellular and Molecular Medicine 10/2014; 18(12). DOI:10.1111/jcmm.12406 · 3.70 Impact Factor
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    ABSTRACT: Adenosine triphosphate (ATP) plays an important role in signal transmission via acting on P2X receptors. P2X7 receptor is involved in pathophysiological changes of ischemic diseases. The PC12 cell line is a popular model system to study sympathetic neuronal function. In this study, the effects of P2X7 on the viability or [Ca2 +]i in PC12 cells after exposure to oxygen-glucose deprivation (OGD) were investigated. The results showed that the viability of PC12 cells was decreased under the condition of OGD. BzATP, a P2X7 agonist, decreased the viability, while P2X7 antiagonist oxATP or P2X7 siRNA reversed the viability of PC12 cells under the condition of OGD. The expression levels of P2X7 mRNA and protein in PC12 cells were up-regulated under the condition of OGD or BzATP treatment. The expression levels of P2X7 mRNA and protein were significantly decreased in OGD PC12 cells, which were pretreated with oxATP or P2X7 siRNA. It was also found that oxATP or P2X7 siRNA effectively suppressed the increase of [Ca2 +]i induced by OGD. P2X7 agonist ATP or BzATP enhanced the [Ca2 +]i rise induced by OGD in PC12 cells. The [Ca2 +]i peak induced by ATP or BzATP in OGD group was decreased by ERK inhibitor U0126. Therefore, P2X7 antagonists or P2X7 siRNA could depress the sympathetic neuronal damage induced by ischemia.
    Autonomic neuroscience: basic & clinical 10/2014; 185. DOI:10.1016/j.autneu.2014.03.006 · 1.37 Impact Factor
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    ABSTRACT: Myocardial ischemia elicits a sympathoexcitatory response characterized by increase in blood pressure and sympathetic nerve activity. Puerarin, a major active ingredient extracted from the traditional Chinese plant medicine Ge-gen, has been widely used in treatment of myocardial and cerebral ischemia. However, little is known about the mechanism. Our study was aimed to explore the effect of puerarin on sympathoexcitatory response induced by myocardial ischemic injury and possible relationship with P2X3 receptor. Our results showed that puerarin alleviated systolic blood pressure and heart rate, and decreased the up-regulated of P2X3 mRNA and protein in SCG of myocardial ischemic rats. The amplitude of ATP-activated currents of SCG neurons was much larger in myocardial ischemic group than that in control group. Puerarin reduced ATP-activated currents in myocardial ischemic group and control group, and the inhibiting effects of puerarin in myocardial ischemic group were stronger than those in control group. Puerarin also significantly inhibited ATP-activated currents in HEK293 cells transfected with P2X3 receptor. These results suggest that puerarin can depress up-sympathoexcitatory response induced by myocardial ischemia via acting on P2X3 receptor in rat SCG to protect myocardium.
    Neurochemistry International 05/2014; 70(1). DOI:10.1016/j.neuint.2014.03.004 · 2.65 Impact Factor
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    ABSTRACT: P2X3 receptors in stellate ganglia (SG) and cervical dorsal root ganglia (DRG) neurons are involved in sympathoexcitatory reflex induced by myocardial ischemic damage. Puerarin, a major active ingredient extracted from the traditional Chinese plant medicine Ge-gen, has been widely used in treatment of myocardial and cerebral ischemia. The present study is aimed to observe the effects of puerarin on the signaling transmission mediated by P2X3 receptor in SG and DRG after myocardial ischemic damage. Our results showed that systolic blood pressure and heart rate increased, and the expression levels of P2X3 mRNA and protein in SG and DRG were up-regulated after myocardial ischemic damage. Puerarin reduced systolic blood pressure and heart rate, relieved pain and decreased up-regulated expression of P2X3 mRNA and protein in SG and DRG after myocardial ischemia. Puerarin inhibited the up-regulated ATP-activated currents in DRG neurons after myocardial ischemia. Thus, puerarin can relieve myocardial ischemic damage through blocking the P2X3 signaling transmission and then depressed the aggravated sympathoexcitatory reflex.
    Brain research bulletin 01/2014; 101. DOI:10.1016/j.brainresbull.2014.01.001 · 2.97 Impact Factor
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    ABSTRACT: Leptin, an adipocytokine produced mainly by white adipose tissue, has a broad role in the regulation of neuronal functions. Accumulating evidence has revealed that leptin plays an important role in influencing neuropathic pain, shown recently by the finding that chronic administration of leptin induced thermal hyperalgesia and mechanical allodynia in naive rats. Chronic constriction sciatic nerve injury (CCI) is a well characterized model used for studying neuropathic pain. The present study was designed to investigate whether leptin plays a role in neuropathic pain in rats induced by CCI by examining particular pain behaviors. After sciatic nerve injury in rats, endogenous levels of leptin and leptin receptor (OB-Rb) were increased in a time dependent manner within the ipsilateral dorsal root ganglion (DRG). Intrathecal administration of leptin once daily for 6 days, beginning 7 days after CCI, alleviated neuropathic pain and decreased the expression of IL-6, TNFalpha, and the P2X2 and P2X3 receptors. Attenuation of endogenous OB-Rb in the DRG by intrathecal administration of OB-Rb antisense oligonucleotides did not change thermal hyperalgesia or mechanical allodynia induced by CCI. Our findings suggest that exogenous leptin can alleviate the chronic neuropathic pain caused by CCI. The leptin effect may be mediated by attenuated expression of IL-6, TNFalpha, and the P2X2 and P2X3 receptors in the DRG of CCI rats.
    Molecular Pain 12/2013; 9(1):65. DOI:10.1186/1744-8069-9-65 · 3.53 Impact Factor
  • Han Liu, Jianuo Liu, Shangdong Liang, Huangui Xiong
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    ABSTRACT: Plasma gelsolin (pGSN), a secreted form of gelsolin, is constitutively expressed throughout the central nervous system (CNS). The neurons, astrocytes and oligodendrocytes are the major sources of pGSN in the CNS. It has been shown that levels of pGSN in the cerebrospinal fluid (CSF) are decreased in several neurological conditions including HIV-1-associated neurocognitive disorders (HAND). Although there is no direct evidence that a decreased level of pGSN in CSF is causally related to the pathogenesis of neurological disorders, neural cells, if lacking pGSN, are more vulnerable to cell death. To understand how GSN levels relate to neuronal injury in HAND, we studied the effects of pGSN on HIV-1 gp120-activated outward K+ currents in primary rat cortical neuronal cultures. Incubation of rat cortical neurons with gp120 enhanced the outward K+ currents induced by voltage steps and resulted in neuronal apoptosis. Treatment with pGSN suppressed the gp120-induced increase of delayed rectifier current (IK) and reduced vulnerability to gp120-induced neuronal apoptosis. Application of Guangxitoxin-1E (GxTx), a Kv2.1 specific channel inhibitor, inhibited gp120 enhancement of IK and associated neuronal apoptosis, similar effects to pGSN. Western blot and PCR analysis revealed gp120 exposure to up-regulate Kv2.1 channel expression, which was also inhibited by treatment with pGSN. Taken together, these results indicate pGSN protects neurons by suppressing gp120 enhancement of IK through Kv2.1 channels and reduction of pGSN in HIV-1-infected brain may contribute to HIV-1-associated neuropathy.
    Molecular and Cellular Neuroscience 11/2013; 57:73–82. DOI:10.1016/j.mcn.2013.10.008 · 3.73 Impact Factor
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    ABSTRACT: Myocardial ischemic injury activates cardiac sympathetic afferent fibers and elicits a sympathoexcitatory reflex by exciting sympathetic efferent action, with resultant augmentation of myocardial oxygen consumption, leading to a vicious cycle of exaggerating myocardial ischemia. P2X7 receptor participates in the neuronal functions and the neurological disorders. This study examined the role of P2X7 receptor of superior cervical ganglia (SCG) in sympathoexcitatory reflex. Our results showed that the expression of P2X7 receptor at both mRNA and protein in SCG was increased after myocardial ischemic injury. P2X7 receptor agonists at the same concentration activated much larger amplitudes of the currents in the SCG neurons of myocardial ischemic rats than those in control rats. P2X7 receptor antagonist (brilliant blue G, BBG) significantly inhibited P2X7 receptor agonist-activated currents in the SCG neurons. Excessive phosphorylation of MAPK ERK1/2 upon the activation of P2X7 receptor might be a mechanism mediating the signal transduction after myocardial ischemic injury. Therefore, the sensitized P2X7 receptor in SCG was involved in the nociceptive transmission of sympathoexcitatory reflex induced by myocardial ischemic injury.
    Neurochemistry International 06/2013; 63(3). DOI:10.1016/j.neuint.2013.06.003 · 2.65 Impact Factor
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    ABSTRACT: P2X receptors participate in cardiovascular regulation and disease. After myocardial ischemic injury, sensory-sympathetic coupling between rat cervical DRG nerves and superior cervical ganglia (SCG) facilitated sympathoexcitatory action via P2X7 receptor. The results showed that after myocardial ischemic injury, the systolic blood pressure, heart rate, serum cardiac enzymes, IL-6, and TNF-α were increased, while the levels of P2X7 mRNA and protein in SCG were also upregulated. However, these alterations diminished after treatment of myocardial ischemic (MI) rats with the P2X7 antagonist oxATP. After siRNA P2X7 in MI rats, the systolic blood pressure, heart rate, serum cardiac enzymes, the expression levels of the satellite glial cell (SGC) or P2X7 were significantly lower than those in MI group. The phosphorylation of ERK 1/2 in SCG participated in the molecular mechanism of the sympathoexcitatory action induced by the myocardial ischemic injury. Retrograde tracing test revealed the sprouting of CGRP or SP sensory nerves (the markers of sensory afferent fibers) from DRG to SCG neurons. The upregulated P2X7 receptor promoted the activation of SGCs in SCG, resulting in the formation of sensory-sympathetic coupling which facilitated the sympathoexcitatory action. P2X7 antagonist oxATP could inhibit the activation of SGCs and interrupt the formation of sensory-sympathetic coupling in SCG after the myocardial ischemic injury. Our findings may benefit the treatment of coronary heart disease and other cardiovascular diseases.
    Purinergic Signalling 06/2013; 9(3). DOI:10.1007/s11302-013-9367-2 · 3.51 Impact Factor
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    ABSTRACT: Purinergic signaling has been found to participate in the regulation of cardiovascular function. In this study, using a rat myocardial ischemic injury model, the sympathoexcitatory reflex mediated by P2X7 receptor via sensory-sympathetic coupling between cervical dorsal root ganglia (DRG) nerves and stellate ganglia (SG) nerves was explored. Our results showed that the systolic blood pressure, heart rate, serum cardiac enzymes concentrations, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) concentrations were increased, and the expression levels of P2X7 mRNA and protein in DRG and SG were up-regulated after myocardial ischemic injury. Administration of brilliant blue G (BBG), a selective P2X7 antagonist, decreased the elevation of systolic blood pressure, heart rate, serum cardiac enzyme, IL-6 and TNF-α, and inhibited the up-regulated expression of P2X7 mRNA and protein in DRG and SG after myocardial ischemic injury. Retrograde tracing test showed that there were calcitonin gene-related peptide sensory nerves and substance P sensory nerves sprouting from DRG to SG, which played an important role in the development of myocardial ischemic injury. The up-regulated P2X7 receptor expression levels on the surface membrane of satellite glial cells contributed to the activation of sensory-sympathetic coupling, which in turn facilitated the sympathoexcitatory reflex. BBG can inhibit the activation of satellite glial cells and interrupt the generation of sensory-sympathetic coupling in the cervical sympathetic ganglia after the myocardial ischemic injury. Taken together, these findings may provide a new therapeutic approach for treating coronary heart disease, hypertension and other cardiovascular diseases.
    Brain research bulletin 05/2013; 96. DOI:10.1016/j.brainresbull.2013.05.004 · 2.97 Impact Factor
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    ABSTRACT: Diabetic neuropathy (DNP) is the most common chronic complication of diabetes. Elevated free fatty acids (FFAs) have been recently recognized as a major cause of nervous system damage in diabetes. P2X receptors play a primary role in regulation of neuronal interleukin (IL)-6 release, which is of paramount relevance to the functional changes of nerve system. The present study aimed to investigate the effects of high FFAs on the P2X7 expression and IL-6 release in PC12 cells. High FFAs induced P2X7 expression and IL-6 release significantly in PC12 cells. Moreover, high FFAs enhanced ATP or BzATP-induced Ca2+ signals in PC12 cells. Inhibition of P2X7 by transfection with P2X7-siRNA or co-culture with BBG (a specific P2X7 inhibitor) at high concentrations of FFAs decreased ATP or BzATP-promoted Ca2+ signals and IL-6 release in PC12 cells. High FFAs induced the phosphorylation of p38 in PC12 cells. Blockade of p38 pathways by SB-203580 inhibited P2X7 up-expression, ATP or BzATP-evoked [Ca2+]i rises as well as IL-6 release in PC12 cells exposed to high FFAs. Therefore, high concentrations of FFAs increased the expression of P2X7 in PC12 cells via activation of p38 mitogen-activated protein kinase (MAPK) signaling pathway, which contributed to P2X7-mediated IL-6 release from PC12 cells.
    Brain research bulletin 02/2013; 94. DOI:10.1016/j.brainresbull.2013.02.002 · 2.97 Impact Factor
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    ABSTRACT: Chemokines and their receptors have the key role in inflammatory responses. The phenomenon of low grade inflammation is associated with the development of type 2 diabetes. Postprandial hyperglycemia increases the systemic inflammatory responses, which promotes the development of type 2 diabetic associating autonomic nervous injuries or cardiovascular disease. Neferine is a bisbenzylisoquinline alkaloid isolated from a Chinese medicinal herb. The objectives of this study will examine the CCL5 and CCR5 expression in the superior cervical ganglion (SCG) of type 2 diabetic rats. The effects of neferine on the expression of CCL5 and CCR5 mRNA and protein in the superior cervical ganglion (SCG) of type 2 diabetic rats will also be observed. The studies showed that in type 2 diabetic rats, body weight, blood pressure, heart rates, fasting blood glucose, insulin, total cholesterol and triglyceride were enhanced and high density lipoprotein was decreased, and CCL5 and CCR5 expression levels in the SCG of type 2 diabetic rats were up-regulated. In type 2 diabetic rats treated with neferine, body weight, blood pressure, fasting blood glucose, insulin, total cholesterol and triglyceride were decreased and high density lipoprotein was increased. The elevated expressions of CCL5 and CCR5 in SCG were decreased after type 2 diabetic rats treated with neferine. The motor nerve conduction velocity (MNCV) in diabetic rats treated with neferine group showed a significantly increment in comparison with that in type 2 diabetic group. Neferine can decrease the expression of CCL5 and CCR5 in the SCG and reduce the SCG neuronal signaling mediated by CCL5 and CCR5 in regulating diabetic cardiovascular autonomic complications.
    Brain research bulletin 10/2012; 90(1). DOI:10.1016/j.brainresbull.2012.10.002 · 2.97 Impact Factor
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    ABSTRACT: Burn injury can induce an inflammatory response in the blood and wound of patients. Procedural activities in burn patients are particularly problematic in burn care due to their high intensity and frequency; hence, procedural pain evoked by burn dressing changes is a common severe issue. Previous studies demonstrated that purinergic signalling is one of the major pathways involved in the initiation, progression and down-regulation of the inflammatory response. Adenosine 5′-triphosphate (ATP) contributes to inflammation, and increased extracellular ATP levels amplify inflammation in vivo via the P2X7 receptor. In the present study, the effect of puerarin, an active ingredient extracted from Chinese herbal medicine Ge Gen, on pain relief of burn patients during dressing change and the mechanism related to the regulation of the purinergic signalling pathway were investigated.
    Burns: journal of the International Society for Burn Injuries 10/2012; 39(4). DOI:10.1016/j.burns.2012.08.013 · 1.84 Impact Factor