Objective To observe the effects of different Mongolian acupuncture methods on neurons form in frontal lobe and NO-cGMP signaling pathways in rats with chronic stress depression; To explore biological mechanism of different Mongolian acupuncture methods for depression.Methods The male SD rats were randomly divided into control group, model group, fluoxetine group, Mongolian silver acupuncture group, Mongolian acupuncture three modulation methods group, and the combination of acupuncture with fluoxetine group (8 rats in each group). Except for control group, other rats were kept alone. Rats receive different treatment 1 hour before stimulations. Behavior changes were observed after 28 days. Hippocampus and frontal lobe tissues were collected. Frontal lobe neurons form changes were observed through different dyeing methods. The content of NO-cGMP was detected by radioimmunoassay and nitrate reductase method.Results Results of Nissl's staining showed that the neuronal pyramidal cells in the frontal lobe of model group rats arranged disorderedly, morphology was not intact and the number was obviously reduced. Nissl's staining got shallow and the most were blurry. The form of the frontal lobe neurons in Mongolian acupuncture three modulation methods group and Mongolian acupuncture group were good, Nissl's staining was dark blue. HE staining results showed that cytomembrane of frontal lobe neurons in model group rats ruptured, and structure was not clear. some cells fell off and formed into cavities. In Mongolian acupuncture three modulation methods group and Mongolian silver acupuncture group, the frontal lobe cells arranged regularly, cellular level was rich, and the nerve cell membrane was complete. The content of NO-cGMP in frontal lobe and hippocampus tissues was significantly elevated in model group. Mongolian acupuncture, Mongolian acupuncture three modulation methods, fluoxetine, and the combination of acupuncture with fluoxetine treatments all could reverse the changes.Conclusion Different Mongolian acupuncture methods may treat depression through regulating and controlling the expression of NO-cGMP.

The effect of electroacupuncture (EA) on TRPM7 mRNA expression of focal cerebral ischemia in rats and further the role of EA in the relationship between TRPM7 and trkA pathway was investigated. Thirty SD rats were randomly divided into 5 groups : normal group, ischemia/reperfusion group, EA treated group (ischemic rats with EA treatment), TE infusion group (ischemic rats with EA treatment and TE buffer infusion), AS-ODN group (ischemic rats with EA treatment and antisense trkA oligonucleotide infusion). The stroke animal model was established by the modified method of middle cerebral artery occlusion. Antisense trkA oligonucleotide that blocked NGFs effects was injected into cerebroventricle before EA. The TRPM7 mRNA was detected by RT-PCR method. The results showed that there were low TRPM7 mRNA levels in cortex and hippocampus in normal group. Compared with normal group, TRPM7 mRNA expression was increased significantly in ischemia/reperfusion group (P<0.05). A significant reduction in the expression of TR-PM7 mRNA was found in EA treated group in contrast to ischemia/reperfusion group (P<0.05). The expression of TRPM7 mRNA in AS-ODN group was remarkably increased compared with EA treated group and TE infusion group (P<0.05). The results indicated that TRPM7 channels in the ischemic cortex and hippocampus in rats might play a key role in ischemic brain injury. EA could reverse the overexpression of TRPM7 in cerebral ischemia/reperfusion rats. And the inhibitory effect of EA on TRPM7 channels might be through trkA pathway.

Summary: The effect of electroacupuncture (EA) on TRPM7 mRNA expression of focal cerebral ischemia in rats and further the role of EA in the relationship between TRPM7 and trkA pathway was investigated. Thirty SD rats were randomly divided into 5 groups : normal group, ischemia/reperfusion group, EA treated group (ischemic rats with EA treatment), TE infusion group (ischemic rats with EA treatment and TE buffer infusion),AS-ODN group (ischemic rats with EA treatment and antisense trkA oligonucleotide infusion). The stroke animal model was established by the modified method of middle cerebral artery occlusion. Antisense trkA oligonucleotide that blocked NGF's effects was injected into cerebroventricle before EA. The TRPM7 mRNA was detected by RT-PCR method. The results showed that there were low TRPM7 mRNA levels in cortex and hippocampus in normal group. Compared with normal group, TRPM7 mRNA expression was increased significantly in ischemia/reperfusion group (P<0.05). A significant reduction in the expression of TRPM7 mRNA was found in EA treated group in contrast to ischemia/reperfusion group (P<0.05). The expression of TRPM7 mRNA in AS-ODN group was remarkably increased compared with EA treated group and TE infusion group (P<0.05). The results indicated that TRPM7 channels in the ischemic cortex and hippocampus in rats might play a key role in ischemic brain injury. EA could reverse the overexpression of TRPM7 in cerebral ischemia/reperfusion rats. And the inhibitory effect of EA on TRPM7 channels might be through trkA pathway.

OBJECTIVE To investigate the effect of arctiin （ARC）relieving lipopolysaccharide （LPS）induced inflammatory injury of human nasopharyngeal epithelial cells NP- 69. METHODS The effects of 24 h treatment of 0.000 1，0.001，0.01，0.1， 1.0，10 μmol/L ARC on the proliferation of NP-69 were determined by MTS method. After 0.01，0.1，and 1.0 μmol/L ARC was applied to NP- 69 for 24 h and NP- 69 was pre-treated with 0.01，0.1 and 1.0 μmol/L ARC for 24 h，and then stimulated with 1.0 μg/mL LPS for 24 h，scratch tests were used to detect cell migration in both experiments. LPS stimulated NP- 69 to establish an inflammation injury model. The levels of nitric oxide （NO），tumor necrosis factor α（TNF-α）interleukin-6（IL-6），and IL- 1β in cell supernatants were detected ，and mRNA and protein expression of zonula oecludens protein 1（ZO-1），β-defensin 3（BD3）， Janus kinase 1 （JAK1），signal transducer and activator of transcription 3 （STAT3） in cell supernatant were also detected. RESULTS Compared with normal group ，0.000 1，0.001，0.01，0.1，1.0，10 μmol/L ARC had no effect on the proliferation of NP-69 after 24 h treatment （P＞0.05）. ARC （0.1，1.0 μmol/L）could significantly promote the rate of cell migration （P＜0.05）. For the inflammatory injure of NP- 69 cells stimulated by LPS ，ARC（1.0 μmol/L）could significantly reduce the release of NO ， TNF-α and IL-6（P＜0.05），significantly increased mRNA and protein expression of ZO- 1 and BD 3 but decreased mRNA and protein expression of STAT 3（P＜0.01 or P＜0.05）. CONCLUSIONS ARC has the effect of reducing the inflammatory injury of NP-69 cells induced by LPS ，promoting the physical and immune defense ability of the nasal mucosa epithelial barrierunder inflammatory environment. The mechanism of action may be related to inhibiting IL- 6/JAK1/STAT3 signaling pathway.