Publications by authors named "Zhen-Yong Gu"

Objective: To explore the role of hydrogen sulfide (H2S) in acute liver injury induced by crushing hind limbs of rats.

Methods: The rats were randomly divided into the following groups: control, crushing, H2S donor sodium hydrosulfide (NaHS) + crushing, H2S inhibitor propargylglycine (PAG) + crushing group. The acute liver injury model was established by 'crushing the hind limbs of rats with standard weight.

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Article Synopsis
  • - The study examines how the stress protein heme oxygenase-1 (HO-1) impacts endoplasmic reticulum stress (ERS) in rat liver cells (hepatocytes) when exposed to lipopolysaccharide (LPS).
  • - Researchers treated cultured rat hepatocyte cells with various combinations of LPS and HO-1 interference methods, measuring cell health and expression of specific stress-related proteins.
  • - Findings indicated that LPS increased HO-1 levels and worsened cell injury and apoptosis; however, blocking HO-1 with siRNA led to even more severe ERS and cell damage, suggesting that HO-1 plays a protective role against LPS-induced injury.
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Objective: To explore the effect of nitric oxide (NO) on the gene expression of hepatic TNF-α and IL-1β by crush injury of rat's soft tissues.

Methods: Rats were randomly divided into sham group, crush group, crush+aminoguanidine (AG) group, and crush+L-arginine (L-Arg) group. Activities of ALT and AST as well as NO level in serum were measured.

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Objective: To observe the time-course expression of calcium-calmodulin dependent protein kinase II delta (CaMK II delta) in cerebral cortex after traumatic brain injury (TBI).

Methods: The TBI rat model was established. The expression of CaMK II delta in cerebral cortex around injured area was tested by Western blotting and immunohistochemical staining.

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In practice of forensic medicine, potential disease can be associated with fatal asphyxia in restraint position. Research has demonstrated that nitric oxide (NO) and nitric oxide synthase (NOS) are plentifully distributed in skeletal muscle, contributing to the regulation of contractile and relaxation. In the current study, respiratory functions, indices of diaphragmatic biomechanical functions ex vivo, as well as NO levels in serum, the expressions of diaphragmatic inducible NOS (iNOS) mRNA, and the effects of L-NNA on contractility of the diaphragm were observed in sepsis induced by cecal ligation and puncture (CLP) under the condition of restraint position.

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Objective: To observe the changes of malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) in rat brain tissue and to explore the mechanism of secondary cerebral injury after brain concussion.

Methods: The brain concussion model was established with the pathological changes of rat brain tissue by Weil stain. The expressions of MDA and SOD in brain tissue were examined by photochemical method.

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Objective: To investigate the role of endoplasmic reticulum stress (ERS) in lipopolysaccharide (LPS)-induced hepatocyte apoptosis.

Methods: Cells of the rat hepatocyte line BRL were cultured. The hepatocytes were treated with LPS, ERS inducer thapsigargin (TG), and ERS inhibitor 4-phenylbutyric acid (4-PBA), respectively or in their different combination.

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Objective: To discuss the myocardial expression of Spry1 and MAPK proteins of viral myocarditis (VMC), to reveal its mechanism of sudden death, and to provide guides for forensic identification of sudden cardiac death.

Methods: Thirty Balb/c male mice were randomly divided into VMC group and control group, inoculated intraperitoneally with Coxsackievirus B3 and Eagel's solution, respectively. After the mice were sacrificed, the cardiac tissues of the mice were taken to proceed regular pathological examination.

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Objective: To observe effects of restraint position on the changes of diaphragmatic mechanical characteristic in rats, and try to explore the role of nitric oxide (NO).

Methods: Rat model of restraint position was established. Rats were divided into control group, restraint position 12h and 24h groups.

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Objective: To observe the effect of soft tissue crush injury on the tensions of thoracic aortic rings (TARs) in rats and to investigate the potential roles of nitric oxide in the change of the tensions.

Methods: Thirty adult SD rats were randomly divided into control group and crush injury (8 h and 16 h after injury) groups. Two kinds of TARs (one with endothelium and the other without endothelium) in vitro were prepared.

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Objective: To investigate the expression of cholecystokinin-octapeptide receptor (CCK-R) mRNA, and observe the effect of lipopolysaccharide (LPS) on CCK-AR mRNA and CCK-BR mRNA expression in ECV-304.

Methods: The human umbilical vein endothelial cell line ECV-304 was cultured and treated with LPS in dosage of 0.01, 0.

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Objective: To investigate the change of nitric oxide (NO) level in local muscles induced by crushing hind-limbs in rats.

Methods: The rat experimental model of hind-limb crushing injury was established by crushing the hind limbs of rats with standard weight for 5 hours, thereafter releving the standard weight for another 5 hours. The rats were randomly divided into sham group, crushing group, crushing and injecting aminoguanidine (AG) group, crushing and injecting L-arginine (L-Arg) group.

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Objective: To investigate the role of oxidative stress in acute liver injury during crushing hindlimbs in rabbit.

Methods: The crushing injury model in rabbit was established by intermittent crushing the hind limbs of rabbit with standard weight. The ALT and AST activities were spectrophotometrically measured.

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Objective: To elucidate the receptor mechanisms underlying the modulation of lipopolysaccharide (LPS)-induced nuclear factor-kappaB (NF-kappaB) expression in human umbilical vein endothelial cell line ECV-304 cells by cholecystokinin octapeptide (CCK-8).

Methods: Human umbilical vein endothelial cell line ECV-304 cells were stimulated with vehicle, LPS, CCK-8 (10(-9)-10(-7) mol/L), CCK receptor non-specific antagonist proglumide, CCK-A receptor (CCK-AR) specific antagonist CR-1409 or CCK-B receptor (CCK-BR) specific antagonist CR-2945 singularly or in combination. The NF-kappaB p65 protein level was determined by Western blot and immunocytochemistry technique.

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Objective: To investigate the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) expression in vascular endothelial cells.

Methods: Human umbilical vein endothelial cell line (ECV-304 cells) was stimulated with vehicle (normal saline) or LPS in the presence (0.01, 0.

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Aim: To investigate the effect of cholecystokinin octapeptide (CCK-8) on the diacylglycerol-protein kinase C (DAG-PKC) signaling pathway in rat pulmonary interstitial macrophages (PIM) stimulated by lipopolysaccaride (LPS).

Methods: The PIM from rat lung tissues were isolated using the collagenase digestion method combined with alveolar lavage and pulmonary vessel perfusion. DAG content and PKC activity were measured by radioenzymatic assay.

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Objective: To investigate the distribution of the polymorphism of the Y-chromosomal loci DYS438, DYS439, GATA A7.1 and GATA A7.2 among Han population in Hebei province.

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Aim: To investigate the effect of lipopolysaccharide (LPS) on the expression and the binding characteristics of cholecystokinin receptors (CCK-R) in rat pulmonary interstitial macrophages (PIMs).

Methods: The PIMs isolated from rat lung tissues were purified by the collagenase digestion method combined with alveolar lavage and pulmonary vessel perfusion. The expression of CCK-R mRNA was detected by RT-PCR and Southern blot analysis and the binding experiments were performed by radioligand binding assay (RBA).

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This study, using cultured bovine pulmonary artery endothelial cells (BPAECs), was undertaken to investigate the roles of endogenous ONOO(-) in LPS-caused injury in endothelial cells. The fluorescent intensity of nitrotyrosine (NT), a specific marker of ONOO(-) generation, in BPAECs represented the content of endogenous ONOO(-) generation. The fluorescent intensity of NT and the number of NT positive cells were detected with flow cytometry (FCM), and the percentage of NT positive cells was calculated.

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To investigate the effect of peroxynitrite (ONOO(-)) on the reactivity of rabbit pulmonary artery, the responses of rabbit pulmonary artery rings (PARs) pre-incubated with ONOO(-) to endothelium-dependent and receptor-dependent relaxants ACh and ADP, endothelium-dependent and receptor-independent relaxant calcium ionophore A23187, endothelium-independent relaxant sodium nitroprusside (SNP) and alpha(1)-adrenoceptor agonist phenylephrine (PE) were observed in vitro in an accumulative manner. (1) Relaxations of PARs to ACh, calcium ionophore A23187 and ADP were markedly impaired with shift of accumulative dose-response curve of each agonist to the right. Inhibition of endothelium-dependent and receptor-dependent or independent relaxation by ONOO(-) was dose-dependent.

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Aim: To elucidate whether CCK receptors exist in lung tissues and their precise cellular localization in the lung.

Methods: CCK-AR and CCK-BR mRNA expression and cellular distribution in the rat lung were detected by highly sensitive method of in situ reverse transcription-polymerase chain reaction (RT-PCR) and conventional in situ hybridization.

Results: CCK-AR and CCK-BR gene positive signals were observed in bronchial epithelial cells, alveolar epithelial cells, pulmonary macrophages and vascular endothelial cells of the rats' lung by in situ RT-PCR.

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For investigation of the regulatory mechanism of cholecystokinin-octapeptide (CCK-8) on pulmonary circulation in rabbits with endotoxic shock (ES) induced by lipopolysaccharides (LPS), mean arterial pressure (MAP) and pulmonary arterial pressure (PAP) were evaluated for 5 h in five groups of rabbits: group of LPS (8 mg/kg, i.v.)-induced ES, group of CCK-8 pretreatment (15 microg/kg, i.

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