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Publications (2)3.23 Total impact

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    ABSTRACT: Painful diabetic neuropathy (PDN) is a common complication of diabetes mellitus and adversely affects the patients' quality of life. Evidence has accumulated that PDN is associated with hyperexcitability of peripheral nociceptive primary sensory neurons. However, the precise cellular mechanism underlying PDN remains elusive. This may result in the lacking of effective therapies for the treatment of PDN. The phenolic glucoside, gastrodin, which is a main constituent of the Chinese herbal medicine Gastrodia elata Blume, has been widely used as an anticonvulsant, sedative, and analgesic since ancient times. However, the cellular mechanisms underlying its analgesic actions are not well understood. By utilizing a combination of behavioral surveys and electrophysiological recordings, the present study investigated the role of gastrodin in an experimental rat model of STZ-induced PDN and to further explore the underlying cellular mechanisms. Intraperitoneal administration of gastrodin effectively attenuated both the mechanical allodynia and thermal hyperalgesia induced by STZ injection. Whole-cell patch clamp recordings were obtained from nociceptive, capsaicin-sensitive small diameter neurons of the intact dorsal root ganglion (DRG). Recordings from diabetic rats revealed that the abnormal hyperexcitability of neurons was greatly abolished by application of GAS. To determine which currents were involved in the antinociceptive action of gastrodin, we examined the effects of gastrodin on transient sodium currents (I(NaT)) and potassium currents in diabetic small DRG neurons. Diabetes caused a prominent enhancement of I(NaT) and a decrease of potassium currents, especially slowly inactivating potassium currents (I(AS)); these effects were completely reversed by GAS in a dose-dependent manner. Furthermore, changes in activation and inactivation kinetics of I(NaT) and total potassium current as well as I(AS) currents induced by STZ were normalized by GAS. This study provides a clear cellular basis for the peripheral analgesic action of gastrodin for the treatment of chronic pain, including PDN.
    PLoS ONE 06/2012; 7(6):e39647. DOI:10.1371/journal.pone.0039647 · 3.23 Impact Factor
  • Hong-ya Zhang · Juan Kang · Wen-juan Han · Meng-meng Hu · Hong-ge Jia
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    ABSTRACT: To investigate TLR4, MyD88 and NF-κB mRNA levels in mouse lymph node with experimental autoimmune myositis(EAM)and determine the role of TLR4 in autoimmune myositis. Thirty femal BALB/c mice were randomly divided into five groups (n=6 animals per group): group 1 was the control, while animals in other four groups were killed at different time point: group 2 in the first week, group 3 in the second week, group 4 in the third week and group 5 in the fourth week since they had been given myosin for preparing EAM. The expressions of TLR4, MyD88 and NF-κB mRNA were measured with real-time fluorescent quantitative polymerase chain reaction. (1)The expressions of TLR4, MyD88 and NF-κB mRNA in each EAM group were significantly high compared with those in the normal control group, which was significantly highest in group 3 of all(P<0.01) and significantly higher in group 4 than in group 5(P<0.01).(2)The expression level of TLR4 mRNA had significant positive correlations with the expressions of MyD88 mRNA and NF-κB mRNA(r=0.906, r=0.967, P<0.01), and the latter two also had significant positive correlations(r=0.919, P<0.01). TLR4 played an important role in the development of autoimmune myositis and run its function mainly by MyD88-dependent pathway that could activate NF-κB for promoting the release of inflammatory factors.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 03/2012; 28(3):272-5.