Effect of acupuncture at Fengchi (GB 20) on the activity of myosin light chain kinase in the middle meningeal artery of migraine modeled rats.

OBJECTIVE: To study the effect of acupuncture at Fengchi (GB 20) on the activation of myosin light chain kinase (MLCK) in the middle meningeal artery of migraine modeled rats. METHODS: Forty-four clean grade healthy female Sprague-Dawley (SD) rats were randomly divided into four groups: the control group, blank control group, Fengchi (GB 20) acupuncture group, and Fengchi (GB 20) prevention group. Neurogenic inflammation of these rats was induced by electrical stimulation. The γ-32P infiltration method was then used to detect MLCK activation in the middle meningeal artery, and immunocytochemistry was applied to detect the structural protein expression of MLCK. RESULTS: The miaraine model was successfully established in the rats. Compared with the control group, MLCK activation was significantly decreased in the blank control group (P < 0.01). CONCLUSION: The activation of MLCK in the middle meningeal artery was increased by acupuncture at Fengchi (GB 20), indicating its effectiveness in preventing and curing on acute migraine attacks.

PTK, ERK and p38 MAPK contribute to impaired NMDA-induced vasodilation after brain injury.

N-Methyl-D-aspartate (NMDA)-induced pial artery dilation is reversed to vasoconstriction following fluid percussion brain injury (FPI). This study investigated the contribution of activation of protein tyrosine kinase (PTK) and the extracellular signal-regulated kinase (ERK) and p38 isoforms of mitogen-activated protein kinase (MAPK) in impaired vasodilation to NMDA after fluid percussion brain injury in pigs equipped with a closed cranial window. NMDA (10(-8), 10(-6) M)-induced vasodilation was reversed to vasoconstriction following fluid percussion brain injury, but such responses were partially restored by genistein (4',5,7-trihydroxy isoflavone), U0126 [1,4-diamino-2,3-dicyano-1,4-bis (0-aminophenylmercapto)butadiene] and SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole], PTK, ERK and p38 MAPK inhibitors (9+/-1% and 16+/-1%, sham control; -6+/-2% and -11+/-3%, fluid percussion brain injury; and 3+/-1% and 6+/-1%, fluid percussion brain injury-genistein, respectively). However, the robustness of the protection to NMDA dilation was significantly greater for U0126 vs. SB203580 (4+/-1% and 7+/-1% vs. 1+/-1% and 1+/-2%). Similar results were observed for glutamate. These data show that PTK, ERK and p38 MAPK activation contribute to impaired NMDA cerebrovasodilation after fluid percussion brain injury. These data suggest that activation of the ERK isoform of MAPK contributes to such impairment more than the p38 MAPK isoform.