ABSTRACT
Objective To investigate the effect of ketamine anesthesia in the early pregnancy on the c-fos mRNA and c-jun mRNA expression in the offsprings of rats. Methods Thirty pregnant SD rats at 5-13 days of gestation were randomly divided into control group and ketamine group (n = 15 each). Ketamine 20 mg/kg was injected intravenously through tail vein followed by 2 h infusion at a rate of 130 mg·kg-1 ·h-1 in ketmine group.While the equal volume of normal saline was given instead of ketamine in control group. The learning and memory function of the offsprings were tested by Morris water maze test on postnatal day 20 and 30. The hippocampal tissues were taken to detect the expression of c-fos mRNA and c-jun mRNA and to observe the ultrastructure. Results Compared with group C, the escape latency was significantly prolonged at 2 days during the test which was performed on postnatal day 30, but there was no significant difference in the expression of c-fos mRNA and c-jun mRNA on postnatal day 20 and 30 and in the indices mentioned above on postnatal day 20 in ketamine group (P ＞0.05). The damage to hippocampal neurons happened in ketamine group. Conclusion The mechanism by which ketamine anesthesia in the early pregnancy inhibits the cognitive function of the offsprings is related to the hippocampal neuron damage, but not related to the expression of c-fos mRNA and c-jun mRNA in hippocampus.
ABSTRACT
Objective To construct replication deficient recombinant adenovirus expressing human c-Jun N-terminal kinase by homologous recombination.Methods The linearized recombinant shuttle vector pAdTrack-CMV-WT-JNK was co-transformed with backbone vector pAdEasy-1 into bacteria BJ5183 for recombinant adenoviral vector.The recombinant adenoviral vector was transfected into HEK293 packing cells to construct replication deficient recombinant adenovirus,and then the recombinant adenovirus was detected by PCR and DNA sequencing.Results JNK recombinant adenoviral vector was effectively transfected into HEK 293 cells and was successfully packed by intracellular enzyme.The expression of green fluorescent protein(GFP)was observed on the 5th day after transfection.The fragment of JNK gene was amplified by PCR and identified by sequencing.The animal experiment confirmed that Ad-WT-JNK was effectivety expressed in liver tissue. Conclusion The research successfully constructed recombinant adenoviral vector and recombinant adenoviral particle.And the achievement laid a foundation for further investigation of the function and application of JNK.
ABSTRACT
Objective To investigate the expression of c-jun in precancerous lesion and squamous cell carcinoma tissues of hamster buckle pouch mucosa.Methods The models of premalignant and malignant lesions were established in hamster buckle pouch mucosa induced with DMBA.The expressions of c-jun in 23 oral normal mucosa, 22 abnormal epithelial hyperplasia and 29 oral squamous cell carcinoma (OSCC) were measured with immunohistochemical SABC method.Results c-jun mainly expressed in basal cells and prickle cells in normal mucosa,simple and abnormal epithelial hyperplasia,its positive expression was in nucleus.c-jun expressed mainly in various layer cells of OSCC,its positive expression was in nucleus and cytoplasm.There were significant differences of positive expression rate between various groups(?2=13.71,P
ABSTRACT
Objective To explore the inhibitory action of antisense c-jun oligodeoxynucleotides(ODN) on matrix metalloproteinase(MMP) expression of fibroblasts induced by ultraviolet B (UVB). Methods The c-jun and c-fos protein expression induced by UVB were measured by Western blot. The mRNA expression of c-jun was determined by reverse transcriptase polymerase chain reaction (RT-PCR) after transfection with c-jun antisense ODN. The pro-MMP-1 and MMP-3 synthesis of fibroblasts was measured by ELISA after treatment with UVB and antisense c-jun ODN. Results The UVB-induced c-jun protein expression of fibroblasts increased to 1.8, 2.6, 3.3 times compared with that of non-irradiated controls,while there was no significant change in c-fos protein expression. The pro-MMP-1 and MMP-3 synthesis induced by UVB irradiation increased obviously. After transfection with different concentrations of c-jun antisense ODN, the UVB-induced c-jun mRNA expression could be significantly inhibited(P
ABSTRACT
Objective To investigate the changes in the expression of Egr-1, C-jun and IL-1? mRNA and protein in the lung injured by mechanical ventilation. Methods Forty male SD rats weighing 250-320 g were randomly divided into 5 groups (n = 8 each): group A received no mechanical ventilation; group B-E received mechanical ventilaion for 30 (B), 60 (C), 90 (D) and 120 (E) minutes. The animals were anesthetized with intraperitoneal 3% pentobarbital 35 mg?kg-1 , tracheostomized and mechnically ventilated (VT =42 ml?kg-1 , RR = 40 bpm, I: E = 1:2, FiO2 = 21 % ) . Arterial blood samples were taken for blood gas analysis. The animals were killed at the end of mechanical ventilation in group B-E and after tracheostomy in group A. The lungs were removed for microscopic examination using HE staining. The expression of Egr-1, C-jun and IL-1? mRNA and protein was detected by RT-PCR and immuno-histochemical technique respectively. Results There was no significant difference in PaO2 and SaO2 among the 5 groups while PaCO2 was significantly decreased in group B and C but increased in group E as compared with group A. The expression of Egr-1, C-jun and IL-1? mRNA and protein was significantly increased by mechanical ventilation in a duration - dependent manner. Histological studies demonstrated that the damage to the lung was correlated with the duration of mechanical ventilation in terms of perivascular inflammatouy cell infiltration, exudates and hemorrhage in the alveoli and thickening of alveolar walls. Conclusion The results of our study show that mechanical ventilation activates and upregulates the expression of the early response genes in a duration - dependent manner. The upregulation of the expression of these genes might be involved in the underlying mechanism of lung damage induced by mechanical ventilation.