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1.
Zhongguo Zhong Xi Yi Jie He Za Zhi ; 37(1): 68-71, 2017 01.
Article in Zh | MEDLINE | ID: mdl-30695428

ABSTRACT

Objective To observe the effect of acupoint application therapy in summer to treat winter diseases (abbreviated as AATSTWD) on nerve-endocrine-immune network system in patients with non-acute attack asthma, and to study possible mechanisms. Methods Fifty healthy volunteers were re- cruited as the normal control group and 50 patients with non-acute attack asthma were recruited as the asthma group. Patients in the normal control group received no intervention. Those in the control group were treated with acupoint application therapy on hot days (applied on the first day of three dog days, 3 times in total). Blood samples were tested before treatment and after 3 times of application. The contents of serum immunoglobulin E (IgE) , interleukin-4 (IL-4) , plasma substance P (SP) , and vasoactive intes- tinal peptide (VIP) were detected using radioimmunoassay. Contents of immunoglobulin A and G (IgA, IgG) were tested by immunoturbidimetry. Content of interferon-y (INF-y) were tested by enzyme linked immunosorbent assay. Results Compared with the normal control group, serum contents of IgA, igG, IFN-y, and plasma VIP decreased, contents of IgE, IL-4, and SP significantly increased in the asthma group before treatment (P <0. 05). Compared with before treatment in the same group, serum contents of IgA, IgG, VIP, and IFN-y increased, and contents of IgE, IL-4, and SP decreased in the asthma group after treatment (P <0. 05). Conclusion Acupoint application therapy in summer to treat winter diseases method could prevent and treat bronchial asthma possibly through improving immune function, control- ling the release of cytokines , and regulating neurotransmitters.


Subject(s)
Acupuncture Points , Asthma , Asthma/therapy , Humans , Immunity, Humoral , Immunoglobulin E , Immunoglobulin G , Seasons
2.
Brain Behav ; 11(8): e2295, 2021 08.
Article in English | MEDLINE | ID: mdl-34337881

ABSTRACT

OBJECTIVE: This study aims to investigate the efficacy of modified Ginseng Yangrong decoction (GSYRD) promoting angiogenesis after ischemic stroke. METHODS: In an in vivo study, rats that survived surgery were allocated into four groups: the control group and model group were treated with normal saline, the GSYRD group was treated with 18.9 mg/kg of GSYRD daily, and the positive control group was treated with Tongxinluo (TXL) (1 g/kg/d). At the end of the seven-day treatment, the area of cerebral infarction, the expression changes of miRNA-210 and ephrin A3 were determined. In an in vitro study, HUVECs were divided into a normal control serum group (NC group), normal control serum OGD group (Oxygen Glucose Deprivation group) (OGD group), OGD + drug-containing serum group (OGD+GSYRD group), and OGD + drug-containing serum + ES group (Endostatin group) (OGD+GSYRD+ES group). The cells in all groups except the NC group were cultured in a sugar-free DMEM medium under hypoxia for 48 h. Cell proliferation, angiogenic structure formation ability, the expression changes of miRNA-210, ephrin A3, and the HIF/VEGF/Notch signaling pathway-related molecules were determined. RESULTS: In vivo, GSYRD significantly reduced infarct size (p < .01), the expression of miRNA-210 and ephrin A3 were decreased in the GSYRD group (p < .05). In vitro, the cell proliferation and tube formation ability were significantly increased in the GSYRD group (p < .05), and the expression of miRNA-210 and ephrin A3 was decreased (p < .05). In addition, in the GSYRD group, the expression of the HIF/VEGF/Notch signaling pathway-related molecules was significantly increased (p < .01 or p < .05). CONCLUSION: GSYRD promotes cerebral protection following angiogenesis and ischemic brain injury. The specific mechanism was activating the HIF/VEGF/Notch signaling pathway via miRNA-210.


Subject(s)
Brain Ischemia , Ischemic Stroke , MicroRNAs , Stroke , Animals , Brain Ischemia/drug therapy , Drugs, Chinese Herbal , MicroRNAs/genetics , Rats , Signal Transduction , Stroke/drug therapy , Vascular Endothelial Growth Factor A
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