Effects of ischemic postconditioning on pneumocyte apoptosis after lung ischemia/reperfusion injury in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effects of ischemic postconditioning (IPostC) on pneumocyte apoptosis after lung ischemia/reperfusion injury in rats.</p><p><b>METHODS</b>Adult male SD rats were randomly divided into 3 groups based upon the intervention (n = 8): control group (C), lung ischemic reperfusion group (LIR), LIR+ IPostC group (IPostC). At the end of the experiment, blood specimens drawn from the arteria carotis were tested for the content of malondialdehyde (MDA), the activity of superoxide dismutase (SOD) and myeloperoxidase (MPO); the pneumocyte apoptosis index (AI) was achieved by tennrminal deoxynucleotidyl transferase mediated dUTP nick end abeling (TUNEL); the expression of Bcl-2, Bax protein in lung tissue was accessed by quantitative immunohistochemistry (MHC) and Bcl-2, Bax mRNA by RT-PCR.</p><p><b>RESULTS</b>IPostC could significantly attenuate the MDA level, MPO activity and improve SOD activity in blood serum which was comparable to I/R and significantly reduced the number of TUNEL-positive cells compared with I/R group, expressed as Al (% total nuclei) from (39.0 +/- 3.46) to (8.0 +/- 0.88) (P < 0.01). The protein and mRNA expression of Bcl-2 and Bax showed that IPO significantly attenuated the ischemia/reperfusion-upregulated expression of Bax protein but improved the expression of Bcl-2 that improved the Bcl-2/Bax ratio (P < 0.01) .</p><p><b>CONCLUSION</b>IPostC may attenuate pneumocyte apoptosis in LIRI by up-regulating expression of Bcl-2/Bax ratio and by inhibiting oxidant generation and neutrophils filtration.</p>

Effect of Xuebijing injection on TLR4--NF-kappaB--IL-1beta pathway of myocardial hypoxia/reoxygenation in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the role of Xuebijing injection(XBJI, traditional Chinese medicine), in inhibiting TLR4--NF-kappaB--IL-1beta pathway of myocardial hypoxia/reoxygenation in rats.</p><p><b>METHODS</b>Thirty six male SD rats (280 +/- 30) g were randomly divided into six groups (n = 6): normal group (N group), balanced perfusion group (BP group), model group (M group), low dose XBJI group (XBJI(L) group), middle dose XBJI group (XBJI(M) group), high dose XBJI group (XBJI(H) group). By Langendorff isolated heart perfusion device to establish the model of myocardial hypoxia/reoxygenation in rats. ELISA was used to detect the concentration of interleukin-1beta (IL-1beta); Western blot was used to detect the expression of nuclear factor kappa B p65 (NF-kappaB p65) protein and toll like receptor 4 (TLR4) protein; and RT-PCR to determine the expression of NF-kappaB p65 mRNA and TLR4 mRNA;To observe microstructure changes of hypoxia/reoxygenation myocardial by light microscopy.</p><p><b>RESULTS</b>Compared with M group, the IL-1beta concentration, NF-kappaB p65 and TLR4 protein,NF-kappaB p65 and TLR4 mRNA of XBJIL group, XBJI(M) group, XBJI(H) group expression decreased in varying degrees,and decreased most obviously all in XBJI(M) group (P < 0.05, P < 0.01); Myocardical structural damage was serious in M group, and improved after treatment XBJI, the most obvious was the XBJI(M).</p><p><b>CONCLUSION</b>Different dose of XBJI can inhibit TLR4--NF-kappaB--IL-1beta signal transduction pathway and reduce several inflammatory reaction after myocardial hypoxia/reoxygenation injury, the 4 ml/100 ml of XBJI is the best.</p>

Effect of Xuebijing Injection on TLR4-NF-κB-TNF-α pathway of rats' myocardial anoxia/reoxygenation / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the role of Xuebijing Injection (XBJI) in inhibiting inflammatory factors associated with anoxia/reoxygenation myocardial inflammatory response of rats.</p><p><b>METHODS</b>Totally 36 healthy male Sprague-Dawley rats, 280 ± 30 g were randomly divided into six groups, i.e., the normal control group (N group), the balanced perfusion group (BP group),the model group (M group),the low dose XBJI group (XBJI(L) group), the middle dose XBJI group (XBJI(M) group),and the high dose XBJI group (XBJI(H) group), 6 in each group. The myocardial anoxia/reoxygenation rat model was established by Langendorff isolated heart perfusion. The concentration of TNF-α in the myocardial tissue was detected by ELISA. The expression of nuclear factor kappa B p65 (NF-κB p65) protein and Toll like receptor 4 (TLR4) protein were detected using Western blot. The expression of NF-κB p65 mRNA and TLR4 mRNA was detected by RT-PCR. Ultrastructural changes of anoxia-reoxygenation rats' heart muscle were observed under transmission electron microscope.</p><p><b>RESULTS</b>Compared with the M group,the TNF-α concentration, expression levels of NF-κB p65 protein and mRNA, TLR4 protein and mRNA decreased to various degrees in the XBJI(L) group, the XBJI(M) group, and the XBJI(H) group. The TNF-α expression level decreased most significantly in the XBJI(L), group (P < 0.01), while other indices decreased most obviously in the XBJI(M) group (P < 0.01, P < 0.05). Expression levels of NF-κB p65 and TLR4 protein were obviously lower in the XBJI(M) group than in the XBJI(L) group (P < 0.05). There was no statistical difference in other indices among the three XBJI groups (P > 0.05). Myocardial fibers were loose and broken with disappearance of transverse striation, and mitochondrial cristae was dissolved and severely damaged in the M group. The aforesaid condition was improved after treated by XBJI, with the most obvious effect obtained in the XBJI(M) group.</p><p><b>CONCLUSIONS</b>Different doses of XBJI could attenuate inflammatory reactions after myocardial anoxia/reoxygenation rats' heart muscle through inhibiting TLR4-NF-κB-TNF-α signal transduction pathway. The best effect could be obtained by 4 mL/100 mL XBJI.</p>

Effect of notoginsenoside Rg1 on p38MAPK expression of pulmonary arterial smooth muscle cells exposed to hypoxia hypercapnia / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To study the effect of Notoginsenoside Rgl on p38 mitogen activated protein kinase (p38MAPK) expression in pulmonary artery smooth muscle cells (PASMCs) cultured in hypoxia hypercapnia.</p><p><b>METHODS</b>SD rat PASMCs was primary cultured, the cells of passage 2- 5 were divided into six groups: normoxic group (N group), hypoxia hypercapnia group (H group), dimethyl sulfoxide (DMSO) control group (HD group), Rg1 treated group (Rg low dose, Rg middle dose and Rg high dose group). Western blot was used to detect the expression of p-p38MAPK protein, and RT-PCR to determine the expression of p38MAPK mRNA.</p><p><b>RESULTS</b>Western blot and RT-PCR analysis indicated that the expression of p-p38MAPK protein and p-p38MAPK mRNA were significantly higher in HD group than those in N group (P < 0.01). Whereas, in Rg1 treated groups, the level of p-p38MAPK markedly decreased (P < 0.01) in dose-dependent manner.</p><p><b>CONCLUSION</b>Notoginsenoside Rg1 has protective effects on PASMCs under hypoxia hypercapnia condition, which may be related to inhibiting expression of p38MAPK.</p>

Cytotoxic effect of aquaporin-4 antibody on in vitro cultured rat cortical cells / 中华神经医学杂志

[Objective]To investigate the cytotoxic effect ofaquaporin-4 (AQP4) antibody onin vitro cultured rat cortical neurons.[Methods]Cortical cells were obtained from Wistar embryonic rats with 16-19-d pregnancy;3 daRer seeding,the cultured cortical cells were randomly divided into a control group and an AQP4 antibody-positive serum treatment group.Neurons of the control group were added the normal human serum and those in the treatment group were added serum from AQP4 antibody positive patients.The number and morphology changes of astrocytes,neurons and microglias were observed by immunohistochemistry at 2,4 and 6 h after being incubated with AQP4 antibody positive serum or controls.[Results] No number or morphology changes of cortical cells were observed in control group at different time points.AQP4 antibody-positive serums induced astrocyte swelling,microglia hyperplasia and neuron axonotmesis,but did not influence the numbers of cortical cells at 2 h after induction.The numbers of astrocytes and neurons in the treatment group (24.73％±5.27％ and 35.49％±8.43％,respectively) significantly decreased as compared with those in the control group (30.34％％:t,4.53％ and 48.60％+10.99％) at 4 h after induction (P＜0.05),while those of microglias in the treatment group (27.35％±13.17％) obviously increased as compared with those in the control group (16.44％±2.70％,P＜ 0.05);these changes became more significant at 6 h after induction.[Conclusion] AQP4 antibodies induce loss of astrocytes and neurons,and microglia activation in primary cortical cells,which maybe imply the primary pathogenic role of AQP4 antibody in neuromyelitis optica.