Liver disease in dogs with tracheal collapse

BACKGROUND: Hepatopathy in dogs with chronic respiratory diseases is poorly recognized. The aim of this study was to evaluate liver parameters alanine transferase, alkaline phosphatase, and glutamate dehydrogenase, as well as basal and stimulated bile acid concentration, in dogs with tracheal collapse. HYPOTHESIS: Dogs with tracheal collapse have hepatopathy. ANIMALS: 26 dogs with tracheal collapse. MATERIALS AND METHODS: Gall bladder contraction was stimulated by intramuscular injection of a synthetic cholecystokinin analogue (ceruletide). Twelve healthy Beagle dogs and 30 dogs of various breeds investigated previously without evidence of hepatic, gastrointestinal, or respiratory diseases served as control. Amelioration of liver variables was assessed after stent implantation. RESULTS: Twelve of 26 (46%) dogs had increased serum activity of 2 or more liver enzymes. Serum basal bile acid concentrations were high in 24 of 26 dogs. Twenty- and 40-minute stimulated bile acids were significantly higher in dogs with tracheal collapse (64.2 +130.0/-43.0 micromol/L and 82.6 +164.0/-57.1 micromol/L) compared to the control dogs (7.0 +/- 3.6 micromol/L and 6.4 +/- 3.5 micromol/L). All twelve dogs reevaluated after a median of 58 days (48-219 days) had a normal breathing pattern and significantly decreased 20 and 40 minutes stimulated bile acids (50.0 +92.7/-32.8 micromol/L, 52.8 +97.6/-34.3 micromol/L; P = .0043), whereas plasma liver enzyme activities were not significantly influenced. CONCLUSION AND CLINICAL IMPORTANCE: There was a significant hepatic dysfunction in the majority of dogs with a tracheal collapse. Liver function should be routinely assessed in dogs with severe respiratory disease.     

Effects of T-cadherin on hypoxia/reoxygenation-induced apoptosis of cardiomyocytes from neonatal rats

AIM: To investigate the mechanism of cardiomyocyte apoptosis induced by hypoxia/reoxygenation (H/R) by silencing a new adiponectin receptor T-cadherin through adenovirus-mediated RNA interference. METHODS: The primary cardiomyocytes were isolated from neonatal rats and cultured for 72 h. The cardiomyocytes were randomly divided into control group, H/R group, APN+H/R group, Ad-T-cadherin-siRNA+APN+H/R group and Ad-HK (adenovirus negative control)+APN+H/R group. The transfection ability and efficiency were examined. The expression of T-cadherin at mRNA and protein levels was detected by RT-PCR and Western blotting. The apoptotic rate was analyzed by flow cytometry and TUNEL. RESULTS: High purity of neonatal rat cardiomyocytes was obtained by primary culture. After 48 h, over 90% of myocardiocytes were infected at MOI=100. The transfected myocardiocytes showed a low expression level of T-cadherin under normal physiological condition. Compared with APN+H/R group, the cell apoptotic rate significantly increased in Ad-T-cadherin-siRNA+APN+H/R group (P<0.05). Compared with H/R group, the difference was not statistically significant (P>0.05). CONCLUSION: Ad-T-cadherin-siRNA effectively infects myocardial cells in vitro and successfully reduces the expression of T-cadherin in myocardial cells. The inhibitory effect of adiponectin on H/R-induced cardiomyocyte apoptosis is attenuated by decreasing the expression of T-cadherin.     

Role of SB203580 in enhancement of hypoxia hypercapnia-induced pulmonary vasoconstriction by voltage-dependent K+ channel blocker 4-aminopyridione in rats

AIM:To investigate the roles of voltage-dependent K+ channel (KV) and p38 mitogen-activated protein kinase (MAPK) signal pathway in the pathological process of hypoxia hypercapnia-induced pulmonary vasoconstriction (HHPV) in rats. METHODS:The second-order pulmonary artery rings isolated from SD rats in vitro was prepared, and randomly divided into control group (N group), hypoxia hypercapnia group (H group), hypoxia hypercapnia+DMSO incubation group (HD group), hypoxia hypercapnia+4-aminopyridione (4-AP) group (4-AP group), hypoxia hypercapnia+SB203580 incubation group (SB group) and hypoxia hypercapnia+4-AP+SB203580 incubation group (4-AP+SB group). Under acute hypoxia hypercapnia condition, the changes of the 3 stages of HHPV incubated by 4-AP or the combined application of 4-AP and SB203580 were observed. At the same time, the tension values of the rings were recorded. RESULTS:Under hypoxia hypercapnia condition, a biphasic pulmonary artery contractile response was observed. The phase II persistent vasoconstriction of the pulmonary artery rings incubated with 4-AP was enhanced. Under hypoxia hypercapnia condition, SB203580 significantly relieved the phase II persistent vasoconstriction induced by 4-AP. CONCLUSION: The KV blocker 4-AP enhances HHPV. SB203580 significantly relieves the phase II persistent vasoconstriction induced by 4-AP, indicating that the participation of p38 MAPK may be one of the important mechanisms for the regulation of HHPV by KV in the rats.     

Role of MAPK inhibition in decrease of hypoxia hypercapnia-induced pulmonary vasoconstriction mediated by Panax notoginseng saponin R1 in rats

AIM：To investigate the role of Panax notoginseng saponin R1 in the pathological process of hypo-xia hypercapnia-induced pulmonary vasoconstriction (HHPV) and to observe the relationship with MAPK signal pathway in rats. METHODS：The model of pulmonary artery ring perfusion in vitro was used, and the rings were divided randomly into the following groups: normoxia group (N group); hypoxia hypercapnia group (H group); H+DMSO incubation group (HD group); H+R1 group, which was divided into 3 subgroups: low-concentration R1 group (RL group), middle-concentration R1 group (RM group) and high-concentration R1 group (RH group); H+SB203580 (p38 MAPK inhibitor) incubation group (S group); H+U0126 (ERK1/2 inhibitor) incubation group (U group); H+R1+SB203580 incubation group (RS group); H+R1+U0126 (RU group). Under acute hypoxia hypercapnia condition, the effects of different concentrations of R1 or R1 at the optimal concentration combined with U0126 or SB203580 on the 3 stages of HHPV were observed. At the same time, the changes of ring tension were recorded via the method of hypoxia hypercapnia condition reactivity. RESULTS：Under the hypoxia hypercapnia condition, a biphasic pulmonary artery contractile response (phase I acute vasoconstriction, phase I vasodilation and phase II persistent vasoconstriction) in the secondary pulmonary artery rings was observed. The treatments in HD group and RL group distinctly relieved the early phase I acute vasoconstriction of HHPV and reversed the phase II persistent vasoconstriction, but the effect in RM group was not obvious. The treatment in RH group enhanced both the early phase I acute vasoconstriction and the phase II persistent vasoconstriction of HHPV. RL and RH groups had significant differences compared with HD group. In contrast to HD group, the values of systolic peak in RS and RU groups decreased dramatically, and the phase II persistent vasoconstriction reversed to relaxation state. The HHPV in RS and RU groups was significantly relieved as compared with RL group. The HHPV in RS and RU groups was relieved as compared with S group and U group. CONCLUSION：R1 at concentration of 8 mg/L relieves acute HHPV in rats. The mechanism may be associated with p38 MAPK and ERK1/2 signaling pathway.     

Panax quinquefolium saponins attenuate hypoxia/reoxygenation-induced injury in rat cardiomyocytes

AIM： To investigate the effects of Panax quinquefolium saponins (PQS) and calcineurin (CaN) signal pathway on cardiomyocyte injury induced by myocardial hypoxia/reoxygenation(H/R). METHODS：Cultured cardiomyocytes isolated from neonatal Sprague-Dawley rats were used to establish the H/R model. The cells were transfected with pCDB-CaN plasmid to overexpress CaN, or exposed to the CaN inhibitor FK506 to interfere the CaN expression. The cardiomyocytes were divided into control group, H/R group, PQS+H/R group, CaN+PQS+H/R group, pCDB+PQS+H/R group and FK506+PQS+H/R group. The apoptosis was analyzed by flow cytometry. The activity of CaN in the cardiomyocytes was detected. The protein expression of CaN was determined by Western blotting. RESULTS：Compared with control group, the apoptosis of the cardiomyocytes in CaN group was significantly increased. Compared with PQS+H/R group, the cell apoptosis, the expression of Bcl-2 and Bax, the activity of CaN and its protein expression in FK506 group were not significantly different. CONCLUSION：Inhibition of CaN activity reduces the H/R injury in cardiomyocytes. However, the mechanism of PQS protecting cardiomyocytes from H/R injury may not be associated with the CaN signaling pathway.     

Expression of hypoxia-inducible factor 1α in human gingival tissues with chronic periodontitis

AIM：To observe the expression of hypoxia-inducible factor 1α (HIF-1α) in human gingival tissues with chronic periodontitis. METHODS：A total of 55 volunteers, including 15 healthy controls, 20 cases of moderate chronic periodontitis and 20 cases of severe chronic periodontitis, were involved in this study, and their gingival specimens were taken and fixed in 4% neutral formalin. The histological changes of gingival tissues were observed by HE staining, and the expression of HIF-1α in gingival tissues was detected by immunohistochemical staining. RESULTS： The proportion of HIF-1α positive cells in gingival tissues was significantly higher in chronic periodontitis groups than that in healthy control group (P<0.01), and that in severe chronic periodontitis group was significantly higher than that in moderate chronic periodontitis group (P<0.05). There was a significantly positive correlation between the severity of chronic periodontitis and the proportion of HIF-1α positive cells in gingival tissues. CONCLUSION：The expression of HIF-1α in human gingival tissues is increased with the severity of chronic periodontitis, suggesting that hypoxia may play an important role in chronic periodontitis.     

HIF-2α在高原动物低氧适应中的研究进展

近年来,全基因组扫描和候选基因分析结果都表明低氧诱导因子调控的信号通路相关基因在藏族群体得到高表达。初步揭示了高原动物对高原低氧环境的适应机制,并发现了一系列对藏族人群适应高原低氧环境发挥作用的候选基因。其中低氧诱导因子-2α(HIF-2α)基因在低氧诱导通路中起着最关键作用,加深对HIF-2α的研究有助于进一步认识藏族人群低氧适应的机制。文中对HIF-2α的结构,分布,表达及调控进行了系统的阐释,并着重对HIF-2α在高原人群中的研究进展进行讨论,还对今后的研究发展方向进行了展望。     

Calcium-sensing receptor mediates hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells through PI3K pathways

AIM:To explore the signal transduction pathways of calcium-sensing receptor(CaSR) that mediates hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells(PASMCs). METHODS:The expression of cyclin D1 and phosphorylated protein kinase B(p-Akt) was analyzed by Western blotting. Cell proliferation was tested using a BrdU incorporation assay, and cell cycle analysis was carried out using a flow cytometric assay. RESULTS:Hypoxia significantly increased the expression of cyclin D1 and p-Akt, the BrdU incorporation and the cell proliferation index. GdCl₃, an agonist of CaSR, amplified the effect of hypoxia. LY294002,a PI3K inhibitor, decreased the up-regulation of cyclin D1 expression and the BrdU incorporation, and also inhibited the increase in the cell proliferation index induced by hypoxia and GdCl₃ in PASMCs. CONCLUSION: The CaSR mediates hypoxia-induced proliferation of rat PASMCs through PI3K pathways.     

Fuzi polysaccharide protects neonatal rat cardiomyocytes with hypoxia-reoxygenation by inhibiting endoplasmic reticulum stress

AIM: To investigate whether the protection mechanism of Fuzi polysaccharide (FPS) is related to inhibition of endoplasmic reticulum stress in cultured neonatal rat cardiomyocytes with hypoxia/reoxygenation (H/R). METHODS: Cultured rat myocardial cells were divided into control group, H/R group (hypoxia for 3 h and reoxygenation for 6 h) and different concentrations of FPS (0.1 g/L, 1 g/L, 10 g/L or 20 g/L) +H/R groups. The cell survival was detected by MTT assay and cell apoptosis of cardiomyocytes was measured by flow cytometry using Annexin V-FITC staining. The expression of glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase-12 were determined by Western blotting. The mRNA expression of CHOP and caspase-12 was detected by quantitative PCR. RESULTS: After reoxygenation, the expression of GRP78, CHOP and caspase-12 in cardiomyocytes was increased. Compared with H/R group, the expression of GRP78, CHOP and caspase-12 in FPS+H/R groups was significantly inhibited, the survival rate of cardiomyocytes was increased and the apoptosis of cardiomyocytes was inhibited. This protective effect of FPS was in a dose-dependent manner and reached its peak at 10 g/L. CONCLUSION: Fuzi polysaccharide protects cardiomyocytes from H/R injury. The mechanism is related to inhibiting endoplasmic reticulum stress.     

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