ABSTRACT
The aim of the present study was to investigate the effects and mechanisms of quercetin on plantar incision-induced matrix metalloproteinase (MMP)-9 and MMP-2 activity,microglia activation and the analgesic effect of quercetin on plantar incision surgery-treated mice.Postoperative pain model was mediated by plantar incision surgery and Von Frey Hairs was used to test the mechanical pain threshold.The activity of MMP-9 and MMP-2 in spinal cord was evaluated by gelatin zymography.The marker of microglia ionized calcium binding adapter molecule 1 (IBA-1),phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) was detected by Western blot.Results showed that quercetin (20,40,80 mg/kg,ip) significantly inhibited plantar incisioninduced mechanical allodynia and suppressed the activity of MMP-9 and MMP-2 in the spinal cord.Moreover,quercetin also markedly inhibited plantar incision-induced up-regulation of IBA-1 and p-p38 in spinal cord.In conclusion,quercetin may alleviate postoperative pain by suppressing MMP-9 and MMP-2 activity in microglia.
ABSTRACT
@#To elucidate possible mechanisms and targets of honokiol(Hnk)for hte treatment of pain, the effects of Hnk on tetrodoxin-senstive(TTX-S)sodium current(INa)were studied in acutely dissociated mouse dorsal root ganglion(DRG)neurons with whole-cell patch clamp technique. Hnk inhibited TTX-S INa currents in a concentration-dependent manner. At 30 μmol/L, Hnk obviously shifted the steady state activation of TTX-S INa toward more positive potentials by 10. 2 mV and prolonged the time course of recovery of sodium current, yet with no significant difference on recovery from inactivation of TTX-S sodium channel.
ABSTRACT
@#The aim of the present study was to investigate the effects and possible mechanism of tetramethylpyrazine(TMP)on morphine-induced microglia activation and tolerance. The antinociception and morphine tolerance were assessed in mice using hot-water tail flick test. IBA-1(ionized calcium binding adapter molecule 1), the marker of microglia, was detected by immumofluorescence method. The expression of p-p38 MAPK and total p38 MAPK(mitogen-activated protein kinase, MAPK)was analyzed by Western blot; real-time polymerase chain reaction(RT-PCR)was used to detect the expression level of tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β). Results showed that TMP(15, 30, 60 mg/kg, ip)inhibited morphine-induced up-regulation of IBA-1, p-p38, TNF-α and IL-1β in a dose-dependent manner, yet with no effect on the expression of total p38 MAPK. In conclusion, TMP significantly inhibited the activation of microglia evoked by morphine via p38 MAPK signaling pathway, thus attenuating morphine antinociception tolerance.
ABSTRACT
AIM To study the characteristic of th e rapidly activating component (Ikr) and the slowly activating compone nt (Iks) of the delayed rectifier K+ current in guinea pig hypertrop hi ed ventricular myocytes induced by thyroxine. METHOD The whole c ell patch clamp techniques were used. RESULTS In hypertrophied ve ntricular myocytes, the magnitude of IKr and IKs were great ly augmented with more positive depolarizations, and the degree of increase of IKr tail and IKs were greater than that of IKr an d IKs tail, respectively. By measuring the amplitude of tail currents which reflected the degree of activation, the activation curve of IKs was shifted toward more negative potential, but that of IKr was marked ly unaffected in hypertrophied myocytes. CONCLUSION Hypertrophied ventricular myocytes induced by thyroxine obviously increased IKr and IKs.
ABSTRACT
Hydrolysate of Meretrix meretrix soft tissue (HMST ) (20, 10g/kg ,po.for 14d ) could markedly inhibit the increase of serum total cholesterol(TC)and triglyceride(TG),enhance the content of high density lipoprotein cholesterol(HLD-C) ;reduced cholesterol(Ch)of the liver(for 28d)in hyperlipimic quail ;and it could also reduce whole blood viscosity in normal and hyperlipemic quail (for 21d).In addition.it could suppress the platelet aggregation induced by ADP in rabbits in vitro. The results show that HMST obviously decreased blood lipid and whole blood viscosity .inhibited platelet aggregation.
ABSTRACT
In cardiac myocytes, Ca 2+ sparks origining fr om a single RyR or a few RyRs are triggered by a single L-type Ca 2+ channel or occur spontaneously. Ca 2+ sparks constitute the elementary local Ca 2+ release events from the SR. Ca 2+ sparks occur at Z-lines and rando mly distribute at different locations, the characteristics of the kinetics are r egulated by many factors. In addition, I Ca.T, Na+/Ca 2+ exchang e, I Ca(TTX) and IP 3 are other putative sources of Ca 2+ that tr igger SR Ca 2+ release.