Objective To know the current status and problems of Traditional Chinese Medicine Clinic and to provide countermeasures.Methods Using literature research and statistical analysis.Results From 2008 to 2014,the number of institutions,health personnel and services of Traditional Chinese Medicine Clinic rose year by year.The Traditional Chinese Medicine Clinic was ahead of TCM-WM Clinic and Minority Clinic.The increase number and increase rate of the number of Traditional Chinese Medicine institutions,health personnel and services are more than TCM-WM Clinic and Minority Clinic.The age constitute is unbalance and the quality of personnel is different in Traditional Chinese Medicine Clinic.Conclusion The government should conduct multi-site practice.Traditional Chinese medicine clinics and other private medical institutions should have the equitable health care treatment.The development in preventive treatment of disease by TCM should be focused on.

[ ABSTRACT] AIM:To illustrate the effect of methylene blue ( MB) on T-lymphocyte subsets and oxidative stress of the thymus in rats with paraquat ( PQ) poisoning.METHODS: Male SD rats ( n=40) were randomly assigned to 4 groups:normal group, control group, low-dose (2 mg? kg-1? d-1 ) MB group and high-dose (4 mg? kg-1? d-1 ) MB group.After 72 h, the pathological morphological changes of the thymus were observed under microscope with HE staining. The SOD activity and MDA content were measured by colorimetry method.The expression of Bcl-2, Bax, CD4 and CD8 was determined by immunohistochemical method.RESULTS:In MB group, the thymus tissue showed good corticomedul-lary demarcation.MDA content decreased and SOD activity increased, indicating that the ability of antioxidation enhanced. Bcl-2 and Bax expression was down-regulated, Bcl-2/Bax ratio increased, and CD4 positive cells increased.CONCLU-SION:MB protects against oxidative damage induced by PQ, and regulates the distribution of T-lymphocyte subsets in the cortex and medulla, thus relieving the persistent body damage.

Aim To evaluate the effects of gavage with lactococcus lactis(L.Lactis) recombinant heme oxyge-nase-1(HO-1) gene on alleviation of intestinal inflammation and protection of the intestinal mucosa in rats with endotoxemia.Methods A model of rats with endotoxemia was produced in 24 healthy SD male rats.The rats were randomly divided into the L.Lactis recombinant HO-1(LL-HO-1)gene group(HO-1 group,n=8),L.Lactis group(LL group,n=8) and glutamine group(Glu group,n=8).The rats received 1 ml(5?1010 CFU?ml-1)?d-1LL-HO-1,1 ml(5?1010 CFU?ml-1)?d-1 L.Lactis or 1 g?kg-1?d-1 glutamine for four days before LPS intraperitoneal injecion.Twenty hours after LPS injection,the full-thickness distal ileum was harvested.The mortality,myeloperoxidase(MPO) activity,the pathological changes,the contents of HO-1,tumor necrosis factor-?(TNF-?) and interleukin-10(IL-10) in the intestine were determined.Results When the results of HO-1 group was compared with those of LL group,the survival rate was significantly elevated in the former(P

Objective To evaluate the effect of emulsified isoflurane post-conditioning on the mitochondrial function during lung ischemia-reperfusion (I/R) in rats in an in vitro experiment.Methods Twenty-four SPF healthy male Sprague-Dawley rats,weighing 250-300 g,were used in the study.After the animals were anesthetized,the lungs were removed,connected to the perfusion system and then divided into 4 groups (n=6 each) using a random number table:control group (group C),group I/R,emulsified isoflurane post-conditioning group (group EI) and intralipid post-conditioning group (group IL).After 20 min of equilibration,the lungs were continuously perfused for 105 min in group C,and the lungs were subjected to 45 min ischemia followed by 60 min reperfusion to establish the model of lung I/R injury in the other three groups.During the reperfusion period,the common perfusate was used in group I/R,the perfusate containing 1.68 mmol/L emulsified isoflurane was used in group EI,and the equal volume of perfusate containing 30％ intralipid was used in group IL.At the end of the equilibration (T0),immediately after beginning of reperfusion (T1) and at 30 and 60 min of reperfusion (T2.3),the arterial oxygen partial pressure (PaO2),airway resistance,pulmonary compliance and tidal volume (VT) were recorded.The right upper lobe of the lung was removed at T3 for determination of wet to dry weight ratio (W/D ratio).The right middle lobe of the lung was removed at T3 for pathologic examination with light microscope.The contents of reactive oxygen species (ROS),NAD+ and ATP in lung tissues were detected.Results Compared with group C,the PaO2,pulmonary compliance and Vr were significantly decreased,and the airway resistance was increased at T1-3,and the W/D ratio and ROS content were increased,and NAD+ and ATP contents were decreased at T3 in I/R,EI and IL groups (P＜0.05).Compared with I/R and IL groups,the PaO2,pulmonary compliance and VT were significantly increased,and the airway resistance was decreased at T2.3,and the W/D ratio and ROS content were decreased,and NAD+ and ATP contents were increased at T3 in group EI (P＜0.05).The pathologic changes of lungs were significantly attenuated in group EI as compared with group I/R.Conclusion The mechanism by which emulsified isoflurane post-conditioning attenuates lung I/R injury is related to decrease in mitochondrial dysfunction in rats in an in vitro experiment.

Objective To evaluate the role of α2 adrenergic receptors in dexmedetomidine-induced inhibition of lipid peroxidation during lung ischemia-reperfusion (I/R) injury in rats.Methods Thirty-two isolated rat lungs in which the model of isolated lung perfusion was successfully established,were divided into 4 groups (n=8 each) using a random number table:control group (C group),I/R group,dexmedetomidine group (D group) and dexmedetomidine plus yohimbine group (DY group).The isolated lungs were subjected to 60 min of ischemia and apnea followed by 75 min of reperfusion and ventilation to establish the model of isolated lung I/R injury.From the beginning of reperfusion,2.3 ng/ml dexmedetomidine was added to the perfusion fluid in D group,and 2.3 ng/ml dexmedetomidine and 0.4 μg/ml yohimbine (an α2 adrenergic receptor blocker) were added to the perfusion fluid in DY group.Lung specimens were obtained immediately after the end of reperfusion for determination of the wet/dry weight ratio (W/D ratio),superoxide dismutase (SOD) activity (by using modified pyrogallol autoxidation method) and malondialdehyde (MDA) content (by thiobarbituric acid method) and for examination of the pathological changes (using haematoxylin and eosin staining).Results Compared with C group,the W/D ratio and MDA content were significantly increased,and the SOD activity was decreased in I/R,D and DY groups (P＜0.05).Compared with I/R group,the W/D ratio and MDA content were significantly decreased,and the SOD activity was increased in D group (P＜0.05).Compared with DY group,the W/D ratio and MDA content were significantly decreased,and the SOD activity was increased in group D (P＜0.05).The pathological changes of lung tissues were significantly attenuated in D group as compared with I/R and DY groups.Conclusion The mechanism by which dexmedetomidine inhibits lipid peroxidation is related to activating α2 adrenergic receptors during lung I/R injury in rats.

Aim To explore the role of AMPK/ PGC-1α pathway in cardioprotection of hydrogen sulfide ( H2 S ) against ischemia/reperfusion ( I/R ) injury. Methods Langendorff perfusion apparatus was used to build an isolated rat myocardial I/R model. Seventy-two male SD rats were randomly divided into 6 groups (n=12):control group (Control), ischemia/reperfu-sion group ( I/R ) , DMSO group ( DMSO ) , inhibitor Compound C group ( CC) , H2 S postconditioning group ( NP) , and H2 S with Compound C group ( N +C ) . The heart rate ( HR ) , the left ventricular developed pressure ( LVDP ) , the maximum rate of increase or decrease of left ventricular pressure ( ± dp/dtmax ) and the left ventricular diastolic pressure ( LVEDP ) were registered at 20 min of baseline and 60 min of reperfu-sion separately. Triphenyl tetrazolium chloride ( TTC) staining and HE staining were used to determine the myocardial infarct size and the myocardial tissue mor-phological change of each group was observed respec-tively. Immunohistochemistry was used to determine the expression of PGC-1α. The expressions of total AMPK ( tAMPKα ) , phosphorylated AMPK ( pAMPKα) and PGC-1α were detected with Western blot anaylsis. Results There were no differences in e-quilibrium hemodyamics observed between the experi-mental groups(P>0. 05). At the end of reperfusion, compared with I/R group, NP group had obviously a-meliorated functional recovery and significantly de-creased myocardial infarct size [ ( 23. 9 ± 3. 4 )% vs (60. 9 ± 3. 8 )%, ( P <0. 05 ) ] . HE staining showed that in NP group, the myocardial injury was reduced. Meanwhile, the expression of pAMPKα and PGC-1αincreased significantly. However, Compound C re-versed the cardioprotection effects provided by hydro-gen sulfide postconditioning and reduced the expression of pAMPKαand PGC-1α. Conclusion AMPK/ PGC-1α pathway is involved in the role of hydrogen sulfide against ischemia/reperfusion injury.

Aim To explore the role of PI3 K/Akt/Sirt1 pathway in cardioprotection of hydrogen sulfide ( H2 S ) postconditioning against ischemia/reperfusion ( I/R) injury. Methods Langendorff perfusion appa-ratus was used to build an isolated rat myocardial I/R model. Isolated rat hearts were subjected to 30 min global ischemia followed by 60 min reperfusion after 20 min of equilibrium. 60 male SD rats were randomly di-vided into 5 groups(n=12):control group(Control), ischemia/reperfusion group( I/R) , H2 S postcondition-ing group( H2 S) , inhibitor LY294002 group( LY) and H2 S with inhibitor group( H2 S+LY) . The left ventric-ular diastolic pressure ( LVEDP ) , the left ventricular developed pressure(LVDP), the maximum rate of in-crease or decrease of left ventricular pressure ( ± dp/dtmax ) were registered at the end of 20 min equilibri-um, 30 and 60 min of reperfusion separately. Triphe-nyl tetrazolium chloride( TTC) staining was used to de-termine the myocardial infarct size. The levels of Sirt1 and PGC-1 mRNA were tested using real-time PCR. The expressions of Sirt1 and PGC-1αwere detected with Western blot analysis. Immunohistochemical method was used to determine the location of Sirt1 . Results There were no differences in equilibrium hemodynamics observed between the experimental groups(P>0. 05). At the end of reperfusion, compared with I/R group, H2 S group had obviously ameliorated functional recov-ery and significantly decreased the myocardial infarct size(26. 9 ± 4. 9)% vs(48. 9 ± 5. 6)%(P <0. 05). Meanwhile, the expression of Sirt1 and PGC-1α in-creased significantly. However,LY294002 reversed the cardioprotective effects provided by hydrogen sulfide postconditioning and reduced the level of Sirt1 and PGC-1α, the percentage of Sirt1-positive nuclei. Con-clusion PI3 K/Akt/Sirt1 signaling pathway mediates the hydrogen sulfide postconditioning-induced protec-tion against I/R injury.

AIM: To investigate the effects of caveolin-1 (Cav-1) scaffolding domain peptide, cavtratin, on lipopolysaccharide (LPS)-induced mouse acute lung injury and heme oxygenase-1 (HO-1) activity.METHODS: Adult male BALB/c mice were randomly divided into 6 groups (n=8 to 10): control, Antennapedia internalization sequence (AP), LPS, LPS+hemin, LPS+ hemin+cavtratin and LPS+hemin+cavtratin+zinc protoporphyrin IX (ZnPP) groups.After LPS administration for 24 h, the lung pathological changes, the wet/dry weight (W/D) ratio of lung tissues, total cell number in bronchoalveolar lavage fluid and serum lactate dehydrogenase activity were measured.The co-localization of HO-1 and Cav-1 was displayed by immunofluorescence, and the HO-1 activity were detected.The mRNA expression of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, MCP-1 and iNOS was detected by real-time PCR.RESULTS: The mice in LPS+hemin+cavtratin group had the decreased interaction between HO-1 and Cav-1, and the increased HO-1 activity compare with LPS group (P<0.05).Compared with LPS group, the pulmonary damage was attenuated in LPS+hemin+cavtratin group, and the injury indexes, including W/D ratio, total cell number in bronchoalveolar lavage fluid and lactate dehydrogenase activity in the serum, and the mRNA expression of inflammatory cytokines all decreased (P<0.05).HO-1 activity inhibitor ZnPP abolished the above protective effect of cavtratin on the lung tissues with LPS-induced acute lung injury.CONCLUSION: Cavtratin has beneficial effects on the lung with LPS-induced acute injury by restoring the HO-1 activity.

AIM:To study the effects of methylene blue (MB) on myocardial ischemia/reperfusion (I/R)-induced mitochondrial injury in isolated rat hearts.METHODS:Spragure-Dawley (SD) rats were divided into 3 groups randomly (n=6): control group, I/R model group and MB treatment group (IR+MB group).The isolated rat hearts were prepared and set up to Langendorff perfusion.The rats in I/R+MB group received MB (2 mg/kg) by intraperitoneal injection 2 h before operation.The hearts in control group were perfused with K-H solution for 110 min consecutively.The hearts in I/R group and I/R+MB group were in equilibrium for 20 min, following by 45 min of global ischemia, and then reperfused for 60 min.The heart rate (HR), left ventricular developed pressure (LVDP), left ventricular pressure maximum change rate (±dp/dtmax) and left ventricular end-diastolic pressure (LVEDP) were recorded.The perfusate was collected to determine the activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH).The contents of reactive oxygen species (ROS), malondialdehyde (MDA) and adenosine triphosphate (ATP), and the activity of superoxide dismutase (SOD) in the myocardial tissues were all determined.Histopathological examination of left ventricle was performed.The mitochondria from the heart tissues was isolated and the mitochondrial swelling and mitochondrial membrane potential (MMP) were analyzed.RESULTS:Compared with control group, the hearts in I/R group showed poorer function, higher CK-MB and LDH levels in the perfusate, increased ROS and MDA contents, higher SOD activity and less ATP content in the heart tissues (P<0.05).Furthermore, the mitochondrial swelling level increased and MMP reduced in I/R group (P<0.05).Compared to I/R group, MB improved heart function and reduced the release of CK-MB and LDH (P<0.05).MB also decreased ROS and MDA contents, and increased the activity of SOD and the content of ATP (P<0.05).In addition, MB alleviated mitochondrial swelling and restored the reduced MMP (P<0.05).CONCLUSION: MB protects the isolated rat hearts from I/R-induced injury by attenuating the damage of mitochondria.