الملخص
<p><b>OBJECTIVE</b>To identify the active material of anti-hepatic fibrosis from Amydae Carapax.</p><p><b>METHODS</b>Membrane separation technology was adopted to screen active fraction in Amydae Carapax, and the active components were isolated from the active fraction using gel chromatography and high performance liquid chromatography. The purified active components in Amydae Carapax were further analyzed using 4700 series time-of-flight mass spectrometer.</p><p><b>RESULTS</b>Proteins and peptides of Amydae Carapax with molecular weight less than 6000 were proved to have biological activity. 8 components (Bj1-Bj8) were isolated from the active fraction. Bj4, Bj6 and Bj7 were screened as active components. Bj7 was further purified, resulting in 7 components (Bj701-Bj707). Bj704 and Bj707 showed significant biological activity. Mass spectrometry showed three molecular ion peaks with highest abundance, i.e. m/e 526, 542 and 572, i.e. m/e 526, 542 and 572, in Bj707 -A The amino acid sequences of above three peptide compounds were NDDY (Asn-Asp-Asp-Tyr), NPNPT (Asn-Pro-Asn-Pro-Thr), and HGRFG (His-Gly-Arg-Phe-Gly), respectively. And M572 was the most abandunt components.</p><p><b>CONCLUSION</b>Three active peptide compounds of anti-hepatic fibrosis of Amydae Carapax were identified.</p>
الموضوعات
Animals , Humans , Cell Line , Liver Cirrhosis , Medicine, Chinese Traditional , Tissue Extracts , Pharmacologyالملخص
<p><b>OBJECTIVE</b>To investigate the effect of Spearmint oil on inflammation, oxidative alteration and Nrf2 expression in rats with chronic obstructive pulmonary disease(COPD).</p><p><b>METHODS</b>COPD model was induced by intratracheal instillation of Klebsiella pneumonia and lipopolysaccharide (LPS) for 12 weeks in rats, and COPD rats were treated with Spearmint oil for 3 weeks. After COPD was induced, the pathological changes, changes in leucocyte number in blood and bronchoalveolar lavage fluid (BALF), MDA in lung homogenate and Nrf2 expression were observed. The effects of Spearmint oil on these changes were determined.</p><p><b>RESULT</b>Spearmint oil 100 mg*kg(-1)significantly reduced leucocyte numbers in BALF, and attenuated bronchiolitis, pulmonary interstitial inflammation and inflammation cell infiltration. Spearmint oil 30-300 mg*kg(-1)decreased the destruction of pulmonary alveolus and the thickness of bronchioles walls, and inhibited goblet cell proliferation. Spearmint oil significantly reduced MDA in lung homogenate, and decreased the expression of Nrf2 protein in lung tissues.</p><p><b>CONCLUSION</b>Spearmint oil has protective effect on lung injury in COPD rats, since it improves pulmonary inflammation,oxidative alteration, and enhances Nrf2 protein expression.</p>
الموضوعات
Animals , Male , Rats , Klebsiella pneumoniae , Lipopolysaccharides , Mentha spicata , Chemistry , NF-E2-Related Factor 2 , Metabolism , Oils, Volatile , Pharmacology , Therapeutic Uses , Oxidative Stress , Pulmonary Disease, Chronic Obstructive , Drug Therapy , Metabolism , Rats, Sprague-Dawleyالملخص
<p><b>OBJECTIVE</b>To investigate the effect of synthetic drug QTY06 on chronic airway inflammation and mucoprotein expression induced by intratracheal (i.t) instillation of lipopolysaccharide (LPS).</p><p><b>METHODS</b>Chronic airway inflammation was induced by i.t instillation of LPS in rats. Phospholipids content and the number of leucocytes in bronchoalveolar lavage fluid (BALF), pathological and immunochemical changes were examined 3 weeks after LPS instillation. The effect of QTY06 on chronic airway inflammation was observed.</p><p><b>RESULT</b>After treatment with QTY06, phospholipids in BALF was significantly increased, and the percentages of neutrophils and lymphocytes were decreased as well as the total number of leucocytes. Compared with the model group, pathological examination showed that tracheitis, bronchitis and pulmonary interstitial inflammation in QTY06 groups were significantly attenuated; epithelial damage was alleviated, infiltration of inflammatory cells reduced and the number of goblet cells decreased. QTY06 significantly decreased MUC5ac expression in trachea and bronchiole epithelium, and reduced the optical density and mucins area (%) as detected by image analysis in rats with chronic airway inflammation.</p><p><b>CONCLUSION</b>QTY06 can reduce and inhibit the chronic airway inflammation induced by LPS in rats, and increase the content of phospholipids in pulmonary surfactant and inhibit the hypersecretion of airway mucins.</p>
الموضوعات
Animals , Male , Rats , Anti-Inflammatory Agents, Non-Steroidal , Pharmacology , Therapeutic Uses , Bronchitis , Drug Therapy , Bronchoalveolar Lavage Fluid , Chemistry , Lipopolysaccharides , Mucin 5AC , Bodily Secretions , Phospholipids , Rats, Sprague-Dawley , Respiratory Mucosa , Bodily Secretionsالملخص
<p><b>OBJECTIVE</b>To explore the mucosal protective effect on the quality of gastric ulcer healing.</p><p><b>METHODS</b>Gastric ulcers were induced in male rats by serosal application of acetic acid. Rats were gavaged for 14 days with saline, omeprazole (OME), teprenone (TEP) and TEP plus OME starting 3 days after ulcer induction. Then the tissues and blood samples were obtained and measured.</p><p><b>RESULT</b>The lower ulcer index (UI) and increased ulcer inhibition rate were observed in OME and OME+TEP groups. In TEP and OME+TEP groups, restored mucosa thickness increased, cystically dilated glands decreased, microvessels in connective tissue increased, the secretion of mucus, hexosamine, PGE(2), bFGF were enhanced, the expression of EGFR was increased.</p><p><b>CONCLUSION</b>TEP can improve the quality of gastric ulcer healing, when combined with OME,the effect is more marked.</p>
الموضوعات
Animals , Male , Rats , Acetic Acid , Anti-Ulcer Agents , Therapeutic Uses , Diterpenes , Therapeutic Uses , Drug Therapy, Combination , Gastric Mucosa , Metabolism , Pathology , Omeprazole , Therapeutic Uses , Rats, Wistar , ErbB Receptors , Secondary Prevention , Stomach Ulcer , Drug Therapy , Pathology , Wound Healingالملخص
<p><b>AIM</b>To observe effects of angiotensin (Ang) II receptor antagonist (AT1) irbesartan and angiotensin-converting enzyme (ACE) inhibitor perindopril on rat myocardium calcineurin expression and sarcoplasmic reticulum Ca(2+)-ATPase activity in the model of pressure-overload cardiac hypertrophy.</p><p><b>METHODS</b>Forty male adult Sprague Dawley rats were divided into 5 groups. One group was treated by sham operation; four groups were myocardium hypertrophy cases caused by banding aortic above renal artery. Drugs were given one week after operation. Group 1: sham group, rats (n=8) were gavaged with normal saline 2 ml/(kg.d) (ig); Group 2: control group, rats (n=8) were treated with normal saline 2 ml/(kg.d) (ig); Group 3: rats (n=8) were given perindopril 2 mg/(kg.d) (ig); Group 4: rats (n=8) were treated with irbesartan 20 mg/(kg.d) (ig); Group 5: rats (n=8) were given irbesartan 20 mg/(kg.d) plus perindopril 2 mg/(kg.d) (ig). Morphometric determination, calcineurin expression and sarcoplasmic reticulum Ca(2+)-ATPase activity were done at the end of 6 week of drug intervention. Expression of calcineurin in myocardium was detected by immunohistochemistry.</p><p><b>RESULTS</b>Left ventricular mass index (LVMI), transverse diameter of myocardial cell (TDM), calcineurin activity were remarkably decreased after drug intervention and this decrease was most remarkable in the combination drug therapy group. Sarcoplasmic reticulum Ca(2+)-ATPase activity was increased after drug intervention, especially in the combined drug therapy group. Calcineurin expression in myocardium was remarkably decreased after drug intervention. LVMI was positively correlated with TDM and calcineurin, negatively correlated with sarcoplasmic reticulum Ca(2+)-ATPase.</p><p><b>CONCLUSION</b>These data suggest that irbesartan and perindopril inhibit cardiac hypertrophy through the increased activity of sarcoplasmic reticulum Ca(2+)-ATPase and decreased expression of calcineurin. Their combination had better effects on regressing of ventricular hypertrophy.</p>
الموضوعات
Animals , Male , Rats , Biphenyl Compounds , Calcineurin , Metabolism , Calcium-Transporting ATPases , Metabolism , Cardiomegaly , Metabolism , Disease Models, Animal , Drug Combinations , Heart , Hypertension , Metabolism , Myocardium , Metabolism , Myocytes, Cardiac , Metabolism , Perindopril , Pressure , Rats, Sprague-Dawley , Sarcoplasmic Reticulum , Tetrazolesالملخص
<p><b>OBJECTIVE</b>To observe the distribution of toll-like receptor 4 (TLR4) in rats' respiratory tract. To study the influence of LPS and Eucalyptus globulus oil on the distribution of TMR4.</p><p><b>METHOD</b>The Sprague-Dawley rats were intratracheally instilled with lipopolysaccharide (LPS,2 mg x kg(-1) per day) for two days to induce acute lung injury. The rats were sacrificed at 72 hours after LPS instillation. Lung morphology was studied. Leukocytes in Bronchoalveolar lavage fluid (BALF) were measured and TLR4 were detected by immunohistochemistry.</p><p><b>RESULT</b>The result of immunohistochemistry showed that TLR4 distributed widely in common rats' respiratory tract. In the group of acute lung injury, the number of leucocyte in BALF was increased apparently, the inflammation in bronchus and bronchioles was more apparently than that of the control group in morphology. And the expression of TLR4 was reinforced in main bronchus and bronchioles. In the group of E. globules oil (300 mg x kg(-1)), the leucocyte number was decreased apparently in BALF, the inflammation was lightened and the expression of TLR4 decreased as compared with the group of models.</p><p><b>CONCLUSION</b>The expression of TLR4 distributes widely in rats' respiratory tract. The stimulation of LPS can reinforce the expression of TLR4. The E. globules oil can reduce the increase of TLR4 induced by LPS in bronchioles.</p>
الموضوعات
Animals , Male , Rats , Anti-Inflammatory Agents, Non-Steroidal , Pharmacology , Bronchi , Metabolism , Bronchoalveolar Lavage Fluid , Cell Biology , Eucalyptus , Chemistry , Leukocyte Count , Lipopolysaccharides , Lung , Pathology , Oils, Volatile , Pharmacology , Plants, Medicinal , Chemistry , Rats, Sprague-Dawley , Respiratory Distress Syndrome , Metabolism , Pathology , Toll-Like Receptor 4 , Metabolismالملخص
OBJECTIVE@#To explore one of evidence for pathologic diagnosis of early myocardial ischaemia.@*METHODS@#Rats were ligated of the left coronary artery according to a previously documented technique, and heart tissue was sampled at different ischaemia time. The expression of CX43 in myocardial cell was detected by Immunohistochemistry.@*RESULTS@#It is showed that the distribution and amount of CX43 positive staining in each group of the myocardial ischaemia was different from that of the control group.@*CONCLUSION@#The changes of CX43 detected by Immunohistochemical methods may be helpful for the diagnosis of early myocardial ischaemia, but further pathologic investigation and research is necessary.
الموضوعات
Animals , Female , Male , Rats , Connexin 43/metabolism , Disease Models, Animal , Forensic Pathology , Immunohistochemistry , Myocardial Ischemia/pathology , Myocytes, Cardiac/metabolism , Myometrium/pathology , Random Allocation , Rats, Sprague-Dawley , Staining and Labeling , Time Factors , Tissue Distributionالملخص
<p><b>OBJECTIVE</b>To explore the mechanisms of muscovite gastric mucosal protective effect.</p><p><b>METHOD</b>Rat model of chronic gastritis were used. After gastric mucosal injury was induced, the rats were divided into 6 groups and were treated with different drugs. 2 weeks later, the tissue and blood samples were obtained and measured.</p><p><b>RESULT</b>The general conditions, the observations under macroscopy, microscope and electron microscope of the middle and high dose of muscovite groups resembled those of the normal group. Their PH levels were higher than those of the model group, and the rates of intestinal metaplasia were lower, but the PGE2 level of the middle dose of muscovite group was the highest.</p><p><b>CONCLUSION</b>Muscovite can be adsorbed on the surface of the gastric mucosa. It has gastric mucosal protective effect by improving excretion of mucus and synthesis of PGE2 in gastric mucosa, restraining gastric acid, reversing of intestinal metaplasia and decreasing inflammation cells.</p>