OBJECTIVETo explore the mechanism of acupuncture combined with medication for treatment of essential hypertension (EH).

METHODSSixty cases of EH were randomly divided into a combined acupuncture and medication group (group A) and a medication group (group B), 30 cases in each one, treated with acupuncture in combination with oral administration of Felodipine, and simple oral administration of Felodipine respectively. Before and after treatment, the changes of blood pressure, and the contents of E-selectin (Es), iNOS and eNOS were determined.

RESULTSAfter treatment, the blood pressure declined in either group. The total effective rate in group A was 86.7% (26/30), which was superior to that of 73.3% (22/30) in group B. After treatment, the plasma Es and iNOS contents in two groups decreased as compared with those before treatment (both P < 0.01), of which, plasma Es content in group A decreased apparently as compared with group B (P < 0.01). After treatment, the content of plasma eNOS increased as compared with that before treatment in group A (P < 0.01).

CONCLUSIONThe mechanism of acupuncture on anti-blood pressure probably relies on the improvements in vascular endothelial cellular function so that Es, iNOS and eNOS expression can be recovered to normal level and ultimately blood pressure is adjusted.

Acupuncture Therapy ; Adult ; Aged ; Blood Pressure ; Combined Modality Therapy ; E-Selectin ; blood ; Felodipine ; therapeutic use ; Female ; Humans ; Hypertension ; blood ; drug therapy ; physiopathology ; therapy ; Male ; Middle Aged ; Nitric Oxide Synthase Type II ; blood ; Treatment Outcome

Adolescent ; Bone Plates ; Fracture Fixation, Internal ; instrumentation ; Fractures, Bone ; diagnostic imaging ; pathology ; physiopathology ; surgery ; Humans ; Male ; Patella ; injuries ; surgery ; Radiography

OBJECTIVETo study the localization and distribution of expressions of Smads (mother against dpp), the intracellular signal transduction molecules in the transforming growth factor-beta (TGF-beta) family, in the testis of male sterile rats with Shen-yang deficiency induced by adenine and to observe the effect of Wenyang Shengjing Decoction (WSD) on these expressions.

METHODSRats were randomly divided into the control group, the model group and the WSD group. Localization and distribution of Smad 1, Smad 2 and Smad 4 expressions were detected by immunohistochemistry SABC and semi-quantitative RT-PCR and analyzed statistically by image analysis system; the contents of testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were detected by radioimmunoassay; and the weights of body, testis and epididymis, as well as sperm number of rats were also measured.

RESULTSSmad 1 and Smad 2 were expressed in cytoplasm of all levels of spermatogenic cells in rats' testis with their positive immuno-responsive substance locating in the cytoplasm, and positive Smad 2 expression could also be found in cytoplasm of Sertoli's cell, but both of them showed negative response in Leydig's cell; Smad 4 was positively expressed in cytoplasm of Leydig's cell but showed negative response in spermatogenic cell and Sertoli's cell. Compared with the normal control, Smad 1 expression was lower (P < 0.05), but Smad 2 and Smad 4 were higher in the model group (both P < 0.05), these abnormal changes could be reversed by WSD treatment (all P < 0.05). Compared with the normal control group, the body weight, sperm number and serum T level were lower, and levels of FSH and LH were higher (all P < 0.05) in the model group, which could all be improved by WSD (P < 0.05); the weights of testis and epididymis were unchanged in all groups (P > 0.05).

CONCLUSIONWSD could not only increase the sperm number through elevating serum T level and decreasing the levels of FSH and LH, but also by way of regulating Smads genes expression to adjust the levels of sex hormones, promote the production of sperm directly or indirectly, so as to treat male infertility.

Animals ; Diagnosis, Differential ; Drugs, Chinese Herbal ; therapeutic use ; Gene Expression ; drug effects ; Immunohistochemistry ; Infertility, Male ; drug therapy ; pathology ; Male ; Medicine, Chinese Traditional ; Phytotherapy ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Smad Proteins ; biosynthesis ; genetics ; Testis ; drug effects ; metabolism ; Yang Deficiency ; drug therapy

OBJECTIVETo observe the effects of TGF-beta on the expression of connexin43 (Cx43) and Cx43-mediated gap junctional intercellular communication (GJIC) in rat Leydig cells, and investigate the association of its effects on Leydig cells with its ability of changing GJIC.

METHODSPrimarily cultured purified Leydig cells were divided into a blank control group, a positive control group (treated with the GJIC inhibitor Carbenoxolone), and four TGF-beta1 groups (treated with TGF-beta1 at the concentration of 1, 2, 5 and 10 ng/ml, respectively, for 20 hours). The localization and expression of Cx43 were detected by immunofluorescence and Western blot, and the changes in GJIC analyzed by FRAP assay.

RESULTSCx43 was expressed as scattered bright spots in the cytoplasm and membrane of Leydig cells. TGF-beta1 significantly elevated the expression of Cx43 in the cytoplasm, but caused no evident change in the membrane. Western blot showed an evident increase in the phosphorylation of Cx43 with the increased concentration of TGF-beta1 as compared with that of the blank control group (P < 0.05). After 20 hours of treatment with TGF-beta1 at 5 ng/ml, the fluorescence intensity of Leydig cells was markedly reduced (P < 0.01), with a mean fluorescence recovery rate of merely (43.58 +/- 1.87)%.

CONCLUSIONTGF-beta1 could significantly down-regulate GJIC between adjacent Leydig cells, and this inhibitory effect may be achieved by promoting the expression of Cx43 in the cytoplasm and elevating the phosphorylation of Cx43.

Animals ; Cell Communication ; drug effects ; Cells, Cultured ; Connexin 43 ; metabolism ; Gap Junctions ; drug effects ; metabolism ; Leydig Cells ; drug effects ; metabolism ; Male ; Phosphorylation ; Rats ; Transforming Growth Factor beta1 ; pharmacology

OBJECTIVETo study the effects of Wenyang Shengjing Decoction (WSD) containing serum on the estradiol (E2) secretion, the synthesized cytochrome P450 aromatase (P450arom) activities, as well as the expression of its encode gene CYP19 in Leydig cells of male sterile rats of adenine induced Shen-yang deficiency (SYD).

METHODSExperimental rats were randomly divided into 4 groups, i.e., the normal control group, the high, middle, and low dose WSD groups, 5 in each group. The normal saline, low, middle, and high dose WSD were respectively given to rats of all groups for 10 successive days. Blood was drawn from rats' heart 2 h after the last gastrogavage. The serum was separated after centrifuge. Leydig cells isolated and purified from SYD rats were primary cultured in vitro and divided into 5 groups in random, i. e., the blank control group, the model group, the high, middle, and low dose WSD groups (1.2, 1.0, and 0.8 g/mL, respectively). The content of E2 released in the culture supernate was determined by radioimmunoassay. The P450arom activity was detected by tritium release assay. Meanwhile, the mRNA and protein expressions of CYP19 were analyzed using fluorescent quantitative PCR and Western blot respectively.

RESULTSCompared with the blank control group, the E2 secretion of the supernate of Leydig cells obviously decreased in the model groups, accompanied with the inhibition of P450arom activities, significant decreased protein and mRNA expressions of CYP19 (P < 0.01, P < 0.05). Compared with the model group, after intervened by WSD containing serum, the E2 secretion in the Leydig cells could be significantly increased, the P450arom activities up-regulated, the CYP19 expressions up-regulated at the protein and mRNA levels partially in a dose-dependent manner (P < 0.01, P < 0.05).

CONCLUSIONSWSD containing serum could effectively elevate the E2 secretion in Leydig cells, which might be partially achieved through up-regulating P450arom activities and enhancing the gene expression of CyP19. This might be one of its mechanisms of action for treating male infertility of SYD.

Animals ; Aromatase ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Estradiol ; secretion ; Leydig Cells ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Serum ; Yang Deficiency ; metabolism

AIMTo study the effect of the recombined human growth hormone(rhGH) on secretory immunoglobulin A (sIgA), epidermal growth factor (EGF) in rats with obstructive jaundice.

METHODSSixty Wistar rats were randomly divided into four groups, sham-operated (group A), common biliary duct-ligated (group B), biliary duct-ligated plus rhGH-treat for one week (group C), biliary duct-ligated plus rhGH-treat for two weeks (group D), each group had 15 rats. Except group A, the rats of other groups were operated with biliary duct-ligated. Until two weeks after operation, the rats of group A and B were killed. After operation, the rats of group C were treated with rhGH hypodermic injection (0.75 U x kg(-1) x d(-1)) for one week, and then killed. The rats of D group were treated with rhGH hypodermic injection (0.75 U x kg(-1) x d(-1)) for two weeks, and then killed. All procedures were performed aseptically. Total bilirubin (TB), alkaline phosphatase (ALP), prealbumin(PA), insulin-like growth factor (IGF-1), sIgA, EGF were measured.

RESULTSCompared with group A, in group B, C, D, serum level of PA, IGF-1 and sIgA, EGF level of gastric and intestinal juice were lower, but TB, ALP were higher, there were significant difference. Compared with group B, the rats with treatment of rhGH in group C and D had higher sIgA and EGF and lower intestinal bacterial translocation.

CONCLUSIONIn objective jaundice rats, rhGH can protect their hepatic function, intestinal physical-barrier function and immune-barrier function, and reduce intestinal bacterial translocation.

Animals ; Bacterial Translocation ; Epidermal Growth Factor ; metabolism ; Growth Hormone ; pharmacology ; Humans ; Immunoglobulin A, Secretory ; metabolism ; Jaundice, Obstructive ; metabolism ; Rats ; Rats, Wistar ; Recombinant Proteins ; pharmacology

OBJECTIVESTo study the expression of Smad1 and Smad5 in the testis of infertile rats with adenine-modeled kidney-yang deficiency and the pathological mechanism of infertility with kidney-yang deficiency, attempting to obtain experimental evidence for the prevention and treatment of male infertility.

METHODSForty-eight 60 d male SD rats were divided randomly into 6 groups with 8 in each: 7 d, 14 d and 21 d kidney-yang deficiency groups, and 7 d, 14 d and 21 d control groups. The experimental rats had been fed with adenine (300 mg/kg) and the expression levels of Smad1 and Smad5 were measured with immunohistochemical SABC method at the 7th, 14th and 21st day.

RESULTSSmad1 immunoreactivity was mainly located in the spermatogonia, spermatocytes and spermatids, and the reactive substance distributed in cytoplasm with negative nuclei. Sertoli cells and Leydig cells were negative. Compared with the control, the expression level of Smad1 was decreased significantly at the 21st day (P < 0.05), but with no significant difference at the 7th and 14th day (P > 0.05). Smad5 immunoreactivity was mainly located in the spermatogonia and spermatocytes, and the reactive substance distributed in cytoplasm with negative nuclei. Compared with the control, the expression level of Smad5 was not significantly different at the 7th day (P > 0.05). The expression of Smad5 was negative at the 14th and the 21st day.

CONCLUSIONThe weaker expression of Smad1 and no expression of Smad5 may be one of the pathological mechanisms of infertility with adenine-modeled kidney-yang deficiency.

Animals ; Infertility, Male ; metabolism ; pathology ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Smad1 Protein ; biosynthesis ; Smad5 Protein ; biosynthesis ; Testis ; metabolism ; Yang Deficiency ; metabolism ; pathology

Objective：To investigate the mechanism of increased glucose uptake, the expression of myoc ardial glucose transporter1 (GLUT1) was determined after low-flow myocardial is chemia. Methods： An in vivo open-chest canine model of low -flow myocardial ischemia was used to correlate myocardial glucose uptake with the number of GLUT1. The expression of myocardial GLUT1 glucose transporter was determined by semiquantitative Northern blotting and immunoblotting. Res ults： GLUT1 mRNA and GLUT1 polypeptide expression was substantially inc reased in ischemic region from the experimental hearts when compared to normal h earts. There was no significant regional difference in GLUT1 expression in eith er normal or ischemic hearts.Conclusion：Myocardial ischemia ind uces a factor or factors which stimulate GLUT1 expression in ischemic myocardial regions. Enhanced GLUT1 expression may be an important protective mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow my ocardial ischemia.

Objective: To investigate whether there is additi ve effects of hyperinsulinemia and ischemia on expression of canine myocardial G LUT4 gene in vivo. Methods: The expression of myocardial GLU T4 was determined by semiquantitative immunoblotting.The expression of GLUT4 mRN A was determined by semiquantitative Northern blotting. Results: Dramatic changes were seen in GLUT4 mRNA and GLUT4 expression in the ischemic hearts.After infusing insulin for 8 h,regional GLUT4 mRNA and GLUT4 levels in is chemic hearts were 2.5, 2.3-fold that of expression in normal hearts(P<0.01 ). Myocardial glucose uptake in ischemic hearts was increased by 4-fold when co mpared with normal hearts(P<0.01). Conclusion: There are not only additive effects of hyperinsulinemia and low-flow ischemia on canine myoc ardial GLUT4 mRNA and GLUT4 expression in vivo, but also increase of myocar dial glucose uptake. Enhanced GLUT4 expression may be an important protective m echanism by which myocardial cells enhance glucose uptake and metabolism during low-flow ischemia.

Objective: To investigate the relationship between serum HGF levels and clinical severity of essential hypertension (EH). Methods: The serum HGF concentrations of 44 patients with EH were measur ed by ELISA. Results: The serum HGF levels in patients with EH w ere higher than that in control. Furthermore, the serum HGF levels of EH patient s with coronary atherosclerosis (CAS) were significantly higher than those of EH patients without CAS ［(920.8±250.0） pg/ml vs （747.9±132.1） pg/ml, P <0.01］ or control ［（643.8±98.2） pg/ml, P<0.01)］.The changes of HGF l evel were correlated with the clinical courses (r=0.63, P<0.01) and stag es (r=0.69, P<0.01) of hypertension. Conclusion: HGF may be considered as a new index for the severity of hypertension and an useful bio chemical parameter for estimating the development of atherosclerosis.