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Objective: To explore the sedative effect of electro-acupuncture on healthy people and its possible mechanism by using EEG power spectral density. Methods: Totally 12 healthy subjects were stimulated by electro-acupuncture at bilateral Zusanli (ST36), Shenmen (HT7) and Sanyinjiao (SP6) acupoints. The multichannel EEG signals induced by electro-acupuncture in electroacupuncture-free state (resting state) and electro-acupuncture state were recorded for 30 minutes respectively. The sedation level of the subjects was monitored by bispectral index monitor (BIS). The power spectrum density (PSD) was employed to analyze the power changes of EEG during electro-acupuncture. Results: Compared with that of the resting state, the BIS value of electro-acupuncture state decreased significantly (P<0.05), the δ band power of EEG signal increased significantly (P<0.05), the α band power of EEG signal decreased significantly (P<0.05). Conclusion: Electro-acupuncture alone can produce sedative effect. The change of EEG activity and the increase of slow wave activity may be related to the sedative effect.
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Objective To observe the curative effect of mouse nerve growth factor and its influence on levels of BDNF,IGF-1,and IL-33 in patients with acute cerebral infarction.Methods Totally 106 cases of patients with acute cerebral infarction were chosen as the research objects between October 2015 and February 2017 in Fourth People's Hospital of Langfang City.According to digital list method,the patients were randomly divided into treatment group and control group,53 cases in each group.The patients in two groups were treated with conventional medicine of acute cerebral infarction,and the patients in treatment group were added to mNGF on the basis of conventional drugs,im injection,18 μg each time,once daily.The patients in control group were not added to NGF treatment,and the patients in two groups were treated for 14 d.Before and after treatment,the degrees of neural function defect in two groups were scored according to NIH Stroke Scale (NIHSS),serum levels of brain-derived neurotrophic factor (BDNF),insulin-like growth factor-1 (IGF-1) and interleukin-33 (IL-33) were determinated using enzyme-linked immunosorbent method.Results Compared with those before treatment,NIHSS scores decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the reduced value in treatment group was obviously higher than that in control group (P ＜ 0.05).After treatment,the total effective rate (93.4％) of treatment group was better than that of control group (46.6％),and the difference was statistically significant (P ＜ 0.05).Compared with before treatment,serum levels of BDNF and IGF-1 rised (P ＜ 0.05),IL-33 decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the changes in treatment group were significantly greater than those in control group (P ＜ 0.05).Conclusion mNGF can effectively reduce the severity of nervous functional defects,and effectively increase expression levels of BDNF and IGF 1 and decreasedexpression level ofIL-33.
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Objective To observe the curative effect of mouse nerve growth factor and its influence on levels of BDNF,IGF-1,and IL-33 in patients with acute cerebral infarction.Methods Totally 106 cases of patients with acute cerebral infarction were chosen as the research objects between October 2015 and February 2017 in Fourth People's Hospital of Langfang City.According to digital list method,the patients were randomly divided into treatment group and control group,53 cases in each group.The patients in two groups were treated with conventional medicine of acute cerebral infarction,and the patients in treatment group were added to mNGF on the basis of conventional drugs,im injection,18 μg each time,once daily.The patients in control group were not added to NGF treatment,and the patients in two groups were treated for 14 d.Before and after treatment,the degrees of neural function defect in two groups were scored according to NIH Stroke Scale (NIHSS),serum levels of brain-derived neurotrophic factor (BDNF),insulin-like growth factor-1 (IGF-1) and interleukin-33 (IL-33) were determinated using enzyme-linked immunosorbent method.Results Compared with those before treatment,NIHSS scores decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the reduced value in treatment group was obviously higher than that in control group (P ＜ 0.05).After treatment,the total effective rate (93.4％) of treatment group was better than that of control group (46.6％),and the difference was statistically significant (P ＜ 0.05).Compared with before treatment,serum levels of BDNF and IGF-1 rised (P ＜ 0.05),IL-33 decreased (P ＜ 0.05) after 14 d of treatment in two groups,but the changes in treatment group were significantly greater than those in control group (P ＜ 0.05).Conclusion mNGF can effectively reduce the severity of nervous functional defects,and effectively increase expression levels of BDNF and IGF 1 and decreasedexpression level ofIL-33.
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<p><b>OBJECTIVE</b>To study the effects of L-arginine (L-Arg) on human colon carcinoma cell line LS174 through NO pathway and the mechanism.</p><p><b>METHODS</b>LS174 cells were cultured in the presence of L-Arg at different concentrations for different time. MTT assay was employed to evaluate the cell proliferation, and the cell morphological changes were observed by optical and electron microscopy. The apoptosis of L-Arg-treated cells was observed by the Annexin V/PI staining. The expression levels of VEGF, COX-2, p53, bcl-2 and bax in the cells were determined using Western blotting and immunocytochemical staining.</p><p><b>RESULTS</b>L-Arg promoted the growth of LS174 cells at a low concentration (0.125 mmol/L) and inhibited the cell growth at higher concentrations (0.5, 2, 8, and 32 mmol/L). Under electron microscope, ultrastructual changes in the cytoplasm and nuclei of LS174 cells were observed 48 h after exposure to L-Arg. Some of the cells showed morphological changes characteristic of cell apoptosis such as cell size reduction, condensation and margination of the nuclear chromatin. Low concentration of L-Arg resulted in a cell apoptosis rate of 2.29%, as compared with the rate of 2.84% in the control group; at higher concentrations, L-Arg caused significantly increased cell apoptosis rates to 26.88%, 28.95%, 63.36%, and 84.51%, respectively. In cells treated with a low concentration of L-Arg, the expressions of VEGF and COX-2 were increased as compared with those in the control cells; higher concentrations of L-Arg obviously decreased the expressions of p53 and bcl-2 and increased the expression of bax.</p><p><b>CONCLUSION</b>Low-concentration L-Arg can promote the growth of LS174 cells probably by up-regulating VEGF and COX-2 protein under the influence of NO, the metabolite of L-Arg. The inhibitory effect of high concentrations of L-Arg is probably mediated by inducing cell apoptosis via NO. The mechanism of L-Arg- induced cell apoptosis may be related to the up-regulation of bax protein and the down-regulation of p53 and bcl-2 proteins.</p>