RESUMO
OBJECTIVE: To observe the effect of moxibustion on epidermal growth factor receptor (EGFR) and phosphorylated extracellular signal regulated kinase 1/2(p-ERK1/2) protein expression in gastric ulcer (GU) rats so as to reveal its mechanisms underlying improving GU. METHODS: Fifty SD rats were randomly allocated to control,model, medication ("Sijunzi" Decoction), non-acupoint moxibustion (non-acup-moxi), and acup-moxi groups (n=10 in each group). The GU model was established by intragastric perfusion of absolute alcohol. Rats of the control group were treated by gavage of distilled water. Rats of the medication group were treated by administration of "Sijunzi" Decoction (8 mL x kg(-1) d(-1)),twice a day for 8 days. Moxibustion intervention was applied to bilateral "Zusanli" (ST 36),"Zhongwan" (CV 12),and "Pishu" (BL 20), "Weishu" (BL 21) alternatively for 30 min, once daily for 8 days. The animals' ulcer index (UI) was assessed by Guth's method, and gastric mucosal pathological changes were observed under light microscope following H. E. staining. The expression of gastric EGFR was detected by immunohistochemistry and that of phosphorylated ERK1/2 (p-ERK1/2) protein determined by Western blot. RESULTS: Compared with the control group, the UI, gastric EGFR and p-ERK1/2 protein expression levels were significantly increased in the model group(P<0.01, P<0.05); whereas in comparison with the model group, the UI was notably decreased in the medication, non-acup-moxi and acup-moxi groups (P<0.05, P<0.01), and EGFR and p-ERK1/2 protein expression levels were further up-regulated in the three treatment groups (P<0.01). The effects of both medication and acup-moxi groups were obviously superior to those of the non-acup-moxi group (P<0.01, P<0.05). No significant differences were found between the medication and acup-moxi groups in the expression levels of EGFR and p-ERK1/2 proteins (P>0.05). Results of H.E. staining showed that alcohol-induced gastric mucosal injury as breakage, exfoliation, inflammatory cell infiltration, etc. was milder in both medication and acup-moxi groups following the treatment. CONCLUSION: Acupoint-moxibustion has a role in relieving alcohol induced gastric mucosal injury in the rat, which may be closely associated with its effects in up-regulating activities of the EGFR/ERK signal transduction pathway.
Assuntos
Receptores ErbB/genética , Proteína Quinase 1 Ativada por Mitógeno/genética , Proteína Quinase 3 Ativada por Mitógeno/genética , Moxibustão , Úlcera Gástrica/genética , Úlcera Gástrica/terapia , Pontos de Acupuntura , Animais , Receptores ErbB/metabolismo , Mucosa Gástrica/enzimologia , Mucosa Gástrica/metabolismo , Humanos , Masculino , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Ratos , Ratos Sprague-Dawley , Úlcera Gástrica/enzimologiaRESUMO
OBJECTIVE: To observe the effect of acupoint-catgut-embedding therapy on blood lipid and insulin levels in type I diabetes mellitus rats;s as to reveal its mechanism underlying improvement of pancreatic functions. METHODS: Thirty SD rats were divided into normal, model and treatment group. The type I diabetes model was established by feeding the rats with high-fat diet and intraperitodneal injection of streptozotocin (STZ). Catgut-embedment was performed in acupoint "Zhongwan" (CV 12)-"Xiawan" (CV 10), "Yishu"-"Ganshu" (BL 18), etc., once every 20 days, twice altogether. Fasting blood glucose (FBG) content was assayed by glucose oxidase method; glycosylated hemoglobin A 1 c (HbA 1 c) assayed by ELISA, and serum fasting C-peptide(FC-p) deterriined by chemiluminescence method; and the triglyceride (TG), total cholesterol (TC), and serum insulin (INS) levels were detected by enzymatic method, separately. The rat's pancreas tissues were fixed with 4% paraformaldehyde and cut into sections (4 Im in thickness) and stained with H. E. method. RESULTS: After modeling, the levels of FBG, HbA 1 c, INS and FC-p, TG, TC were significantly increased in the model group in comparison with those of the normal group (P<0.05), while INS sensitive. index was apparently decreased in the model group (P<0.05). Following catgut-embedding treatment, changes of the above-mentioned indexes were all remarkably reversed (P<0.05), and H.E. staining showed an improvement of the injured pancreatic tissue and islet cells. CONCLUSION: Catgut-embedding therapy can reduce fasting blood glucose and insulin resistance, and improve lipid metabolism in type I diabetic rats, which may contribute to its effect in protecting pancreatic islet cells.
Assuntos
Pontos de Acupuntura , Terapia por Acupuntura , Diabetes Mellitus Tipo 2/terapia , Terapia por Acupuntura/instrumentação , Animais , Glicemia/metabolismo , Categute , Colesterol/metabolismo , Diabetes Mellitus Tipo 2/metabolismo , Hemoglobinas Glicadas/metabolismo , Humanos , Insulina/metabolismo , Lipídeos/sangue , Masculino , Ratos , Ratos Sprague-Dawley , Triglicerídeos/metabolismoRESUMO
OBJECTIVE: To observe the effect of electroacupuncture (EA) stimulation on the expression of metalloprotei- nase-9 (MMP-9) and tissue inhibitor-1 (TIMP-1) in the lung tissue in rats with chronic obstructive pulmonary disease (COPD), so as to reveal its mechanisms in protecting the lung tissue. METHODS: Forty male SD rats were equally randomized into control, model, medication and EA groups. The COPD model was established by smoke-fumigation method (passive smoking in a closed box) and endotracheal injection of lipopolysaccharide (200 microg/100 microL) for 30 days. Rats of the medication group were treated by i.p. of dexamethasone acetate injection (2.0 mg/kg), once daily for 22 days. EA was applied to LU 9, ST 36, ST 40 and KI 3 for 20 min, once daily for 22 days. Pathological changes of the pulmonary tissue were observed under optical microscope after hematoxylin and eosin (H.E.) staining. The expression of pulmonary MMP-9 and TIMP-1 was assayed by immunohistochemistry. RESULTS: H.E. staining showed pulmonary diffuse edema, severe inflammatory cell infiltration, and increase of the numbers of goblet cells, proliferation of fibroblasts, etc. in the model group which were relatively milder in the medication and EA groups. The expression levels of pulmonary MMP-9 and TIMP-1 proteins were significantly higher in the model group than in the control group (P<0.05), and were considerably down-regulated in both EA and medication groups in comparison with the model group (P<0.05). There were no significant differences between the EA and medication groups in MMP-9 and TIMP-1 expression levels (P>0.05). CONCLUSION: EA can effectively suppress the increased expression of pulmonary MMP-9 and TIMP-1 in COPD rats, which may contribute to its effect in improving COPD-induced pathological changes.