Air Pollutants ; toxicity ; Animals ; Female ; Lung ; drug effects ; pathology ; Male ; Nitrogen Dioxide ; toxicity ; Particulate Matter ; toxicity ; Pulmonary Surfactant-Associated Proteins ; metabolism ; Rats ; Rats, Wistar ; Sulfur Dioxide ; toxicity ; Uteroglobin ; metabolism

OBJECTIVETo observe preventive and therapeutic effect of Yifei Jianpi Recipe (YJR) on chronic obstructive pulmonary disease (COPD) model rats and to explore its mechanism from the way of airway inflammation and airway mucus hypersecretion.

METHODSThe COPD rat model was established by using cigarette smoking combined with intratracheal injection of lipopolysaccharide (LPS). Male SD rats were randomly divided into the blank control group (control group), the model group, the YJR group, 6 in each group. Forced vital capacity (FVC), forced expiratory volume in 0. 1 second (FEV0. 1), FEVO. 1/FVC, peak expiratory flow (PEF) was tested by lung function device. Pathological changes of bronchi and lung tissues were observed by HE staining. Airway Goblet cells were observed using AB-PAS staining. Contents of IL-8, IL-17, and TNF-α in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA). Protein expressions of intercellular cell adhesion molecule-1 (ICAM-1), nuclear factor KB (NF-KB), mucin 5AC (Muc5AC), and Toll-like receptor 4 (TLR4) in rat airway were detected by immunohistochemical assay. mRNA expressions of TLR4 and Muc5AC in bronchi and lung tissues were detected by real-time quantitative PCR (RT qPCR).

RESULTSChanges of bronchi and lung tissues in the model group rats were consistent with typical pathological manifestations of COPD. Compared with the model group, the degree of lung injury was significantly alleviated in the YJR group. Compared with the control group, FVC, FEV0. 1, FEVO. I/FVC, and PEF were decreased (P <0. 01), contents of IL-8, IL-17, and TNF-α in BALF were significantly increased (P <0. 01), protein expressions of ICAM-1, NF-KB, Muc5AC, and TLR4, mRNA expression levels of Muc5AC and TLR4 in bronchi and lung tissues were also significantly increased in the model group (P <0. 01). Compared with the model group, FVC, FEV0. 1, FEV0. 1/FVC, and PEF were significantly increased in the YJR group (P <0. 01, P <0. 05), but the rest indices were significantly lowered (P <0. 01, P <0. 05).

CONCLUSIONYJR could decrease contents of IL-8, IL-17, and TNF-α in BALF of COPD model rats, inhibit protein expression levels of ICAM-1, NF-κB, Muc5AC, and TLR4.in airway and lung tissues, thus playing preventive and therapeutic roles by reducing airway inflammation and airway mucus hypersecretion.

Animals ; Bronchi ; Bronchoalveolar Lavage Fluid ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Inflammation ; Intercellular Adhesion Molecule-1 ; metabolism ; Interleukin-17 ; metabolism ; Interleukin-8 ; metabolism ; Lipopolysaccharides ; Lung ; Male ; Models, Animal ; Mucin 5AC ; metabolism ; Mucus ; metabolism ; NF-kappa B ; metabolism ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Toll-Like Receptor 4 ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

Objective To observe the expressions of matrix metalloproteinase 1(MMP1) and tissue inhibitor of matrix metalloproteinase1(TIMP1) and the collagen type Ⅰ,Ⅲ deposition in the liver tissues,and evaluate the possible fibrosis mechanism of patients with chronic hepatitis B(CHB) in the way of degradation of collagen. Methods The specimens of the biopsy liver in 50 cases with CHB were detected for the expressions of type Ⅰ,Ⅲ collagen proteins,MMP1 and TIMP1 by immunohistochemical staining. Results The expressions of type Ⅰ,Ⅲ collagen proteins and TIMP1,were significantly increased along with the advancing of hepatic fibrosis.There was a positive correlation between the expressions of type Ⅰ,Ⅲ collagen proteins and TIMP1. Conclusions Hepatic fibrosis in the patients with CHB may be related to increase of TIMP1 expression that inhibit the degradation of collagen.

[ABSTRACT]AIM:Toobservetheeffectofazithromycinontheratswithchronicobstructivepulmonarydisease ( COPD) , and to explore the underlying mechanism about the airway inflammation and mucus hypersecretion.METH-ODS:Male SD rats were randomly divided into normal control group, COPD model group, azithromycin treatment group. The COPD model was established by the method of cigarette smoking combined with intratracheal injection of LPS.Patho-logical changes of the bronchi and lung tissues of the rats were observed with HE staining.Pulmonary ventilation function in the rats was detected with pulmonary function instrument.The levels of IL-8, IL-17 and TNF-αin bronchoalveolar lavage fluid (BALF) were measured by ELISA.The expression of MUC5ac and TLR4 at mRNA and protein levels in bronchi and lung tissues was determined by real-time PCR and Western blot.RESULTS:HE staining showed that the changes of bron-chi and lung tissues in model group were consistent with typical pathological manifestations of COPD .Compared with model group, these changes were alleviated in treatment group.The pulmonary functions in model group were significantly de-creased compared with control group.The levels of IL-8, IL-17 and TNF-αin the BALF in model group were significantly increased compared with control group (P<0.05).The expression of MUC5ac and TLR4 at mRNA and protein levels in model group was significantly higher than that in control group (P<0.05).Compared with model group, the degree of the descent in pulmonary function in treatment group was significantly lessened.Compared with model group, the levels of IL-8, IL-17 and TNF-αin treatment group were significantly inhibited (P<0.05).Furthermore, the expression of MUC5ac and TLR4 at mRNA and protein levels in treatment group was significantly lower than that in model group ( P<0.05 ) . CONCLUSION:Azithromycin decreases the levels of IL-8, IL-17 and TNF-αin the BALF of COPD model rats, inhibits the protein expression of MUC5ac and TLR4 in the lung tissues, thus playing a preventive and therapeutic role to reduce airway inflammation and airway mucus hypersecretion.

OBJECTIVE To observe the regulation effect of chidamide on energy metabolism in HCT-8 and HT-29 cells. METHODS HCT-8 and HT-29 cells were treated with chidamide 5,10 and 20 μmol · L-1. Morphological changes of these cells were observed under an ordinary optical microscope. Cell proliferation was detected by MTT. ATP production was determined by CellTiter-Glo? assay kit. Metabolic changes were tested by glycolytic stress kit. The mRNA level of lactate dehydrogenase A (LDH-A)was analyzed by real-time quantitative PCR,whereas the protein level of LDH-A was analyzed by Western blotting. RESULTS Compared with control group,cell morphology of HCT-8 and HT-29 cells in chidamide treated group was irregular,accompanied by deformation,shrinkage and cell debris, and the inhibitory rate of proliferation increased(P<0.05). There was no significant difference in ATP total content between chidamide 5 and 10 μmol · L-1 16 h treatment groups,but in chidamide 20 μmol · L-1 treatment group it was decreased(P<0.05). Chidamide 20μmol · L-1 had no effect on oxygen consumption rate, but glycolysis ATP generation rate was reduced by 30.7% and 37.9%(P<0.05),respectively. Chidamide 20μmol · L-1 had no effect on LDH-A mRNA level,but it decreased the protein level of LDH-A(P<0.01). CONCLUSION Chidamide can abate the respiratory metabolic ability of HCT-8 and HT-29 cells. The mechanism may be related to the down-regulation of LDH-A.

OBJECTIVEAfter sinboneHT bone replacement (SBR) was implanted in animals, to evaluate the biocompatibility of SBR and compounded in autogenetic bone in the proportion of one to one in order to prepare for the clinical applications in the future.

METHODSBone defects of 10 mm x l0 mm x 2 mm was made at the mandibular of rabbits, then SBR with different granule diameter and autogenetic bone was compounded in the proportion of being applied in the left defects, while autogenetic bone was implanted in the right defects and nothing was used in the right reformed defects. Animals were sacrificed at 2, 4 and 8 weeks respectively. The biologic capacity was evaluated with anatomy, X-rays studies and histology.

RESULTSSBR has better biocompatibility, which can effectively accelerate the reconstruction of bone defects and help the new bone by being compounded with autogenetic bone. It provides the appropriate scaffold or template which would allow cellular infiltration, attachment and multiplication.

CONCLUSIONSBR is a kind of bone substitute material with good biocompatibility. SBR compounded with self-bone has a better regeneration function.

Animals ; Bone Regeneration ; Bone Substitutes ; Mandible ; Rabbits ; Reconstructive Surgical Procedures

OBJECTIVETo study the effect of Danshensu (DSS) and Ligustrazine (TMZ), the extracts of Chinese herbs for promoting blood circulation, on angiotensin II (Ang II) induced myocardial hypertrophy and its related genes, and to explore the mechanisms of inhibitory effect.

METHODSAdopting one-step method, the total RNA of myocardial cells was extracted by TRIzol reagent. Then the expression of ANP and beta-actin mRNA, as symbol of myocardial cells, were detected by RT-PCR.

RESULTSMolecular biological research showed that Ang II could significantly increase the expression of ANP mRNA in myocardial cells (P < 0.01), which could be significantly inhibited by Losartan (P < 0.01), both DSS and TMZ had the inhibitory effect (P < 0.05). Ang II could increase beta-actin mRNA expression in myocardial cells simultaneously, Losartan, DSS and TMZ could also significantly inhibit it (P < 0.05).

CONCLUSIONThe effective ingredients of Chinese herbs for promoting blood circulation, DSS and TMZ, have the effect of inhibiting the hyper-expression of ANP and beta-actin induced by Ang II, and preventing myocardial hypertrophy, therefore, it could be used to prevent and treat cardiomegaly.

Angiotensin II ; Animals ; Animals, Newborn ; Atrial Natriuretic Factor ; biosynthesis ; genetics ; Cardiomegaly ; chemically induced ; metabolism ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Female ; Lactates ; pharmacology ; Male ; Myocytes, Cardiac ; cytology ; metabolism ; Pyrazines ; pharmacology ; RNA, Messenger ; biosynthesis ; genetics ; Rats ; Rats, Wistar

OBJECTIVETo explore the therapeutic effect of qi benefiting blood activating method (QB-BAM) on acute exacerbation of chronic obstructive pulmonary disease (AECOPD) patients with blood stasis syndrome (BSS) by observing its effect on plasma fibrinogen (Fg) and D-dimer (D-D) levels.

METHODSSixty AECOPD patients with BSS were randomly assigned to the treated group and the control group, 30 in each group. All patients received conventional therapy for AECOPD. Those in the treated group were additionally injected with Shengmai Injection and Tanshinone IIA Injection. Clinical efficacy and indices including levels of Fg, D-D, PaO2, and PaCO2 were measured and compared before and after treatment.

RESULTSThe effective rate was 93.3% (28/30 cases) in the treated group, higher than that of the control group [73.3% (22/30 cases) , P < 0.05]. There was no significant difference in all indices between the treated group and the control group before treatment (P >0.05). After treatment all indices were significantly improved in the two groups (P < 0.01). But in the treated group levels of Fg and D-D decreased more and levels of PaO2 increased more (P < 0.01). Plasma levels of Fg and D-D levels were negatively correlated with PaO2 (r = -0.493, r = -0.438, P < 0.01) before treatment, and also negatively correlated with PaO2 (r = -0.452, r = -0.325, P < 0.01, P < 0.05) after treatment, but they were not significantly correlated with PaCO2 before and after treatment (P >0.05).

CONCLUSIONSQBBAM could play a therapeutic role in improving prethrombotic states of AECOPD patients with BSS. Plasma levels of Fg and D-D were related to the severity of AECOPD.

Acute Disease ; Drugs, Chinese Herbal ; therapeutic use ; Fibrin Fibrinogen Degradation Products ; Fibrinogen ; Hemostatics ; Humans ; Plasma ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; Qi

Objective To observe expressions of ?-smooth muscle actin(?-SMA) and collagen type Ⅰ,Ⅲ deposition in the liver tissues, and to evaluate potential mechanism of fibrosis in patients with fibrosing cholestatic hepatitis (FCH) by collagen synthesis. Method Immunohistochemical staining was used to detect the expressions of ?-SMA and contents of type Ⅰ,Ⅲ collagen proteins, which were from the specimens of the biopsy liver in 9 cases with FCH associated with hepatitis virus B (HBV) developed following renal transplantation and in 5 cases without liver disease(control group), respectively. Results The expressions of ?-SMA and type Ⅰ,Ⅲ collagen proteins in the patients with FCH were significantly higher than those in the control group. The expression and distribution pattern of ?-SMA and type Ⅰ,Ⅲ collagen proteins were almost identical, and quantitative analysis showed a positive correlation (P

Objective To explore the mechanism of percutaneous laser disc decompression (PLDD) for treating prolapse of intervertebral disc. Methods 15 rabbits were divided into 3 groups randomly: sham group, model group with PLDD treatment, model group without PLDD treatment. The nerve conduction velocity (NCV) of L6 nerve root and the activity of phospholipase A2 (PLA2) in the intervertebral disc of L5-6 were determined 2 weeks after the initial surgery. Results NCV in the group with PLDD was significantly faster than that in the group without PLDD (P<0.001); NCV in the group without PLDD was significantly lower than that in the sham group (P<0.001). The activity of PLA2 in the group with PLDD was significantly lower than that in the group without PLDD (P<0.001); The activity of PLA2 in the group without PLDD was significantly higher than that in the sham group (P<0.001). Conclusion The activity of PLA2 in the herniated discs is higher than that in normal discs, which result in NCV falls remarkably. The PLDD can reduces chemical factors such as PLA2.