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OBJECTIVES@#To explore the expressions of c-fos and c-myc in skin lesion of cutaneous squamous cell carcinoma (CSCC).@*METHODS@#Using retrospective analysis, 73 cases of CSCC were selected from Department of Dermatology, the Second Affiliated Hospital of Xi'an Jiaotong University, which were removed between January 2000 and January 2012. It was considered as experimental group. Meanwhile, 11 cases of normal skin specimens of non tumor patients were selected as control group. The expression level of c-fos and c-myc was compared in the two groups.@*RESULTS@#The expressions of c-fos [72.60% (53/73)] and c-myc [83.56% (61/73)] in experimental group were statistically significant (P≤0.05) compared with control group (0%). Expression of c-myc protein was negatively related to differentiation of CSCC. The difference was statistically significant (χ(2)=7.26, P=0.001<0.05). While expression of c-fos protein was positively related to differentiation of CSCC, which was statistically significant (χ(2)=7.47, P=0.001 2<0.025).@*CONCLUSIONS@#The expression level of c-fos and c-myc can be used as an important indicator of CSCC differentiation, and it has closely connection with the differentiated degree, which can guide clinical prognosis.
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AIM: To investigate the effect of extracellular signal-regulated kinase 1/2 signaling pathway after severe diffuse brain injury (DBI) in rats, and to provide base for treatment. METHODS: Male Sprague-Dawley rats were randomly divided into four groups: control group, traumatic group, low dose of inhibitor U0126 treatment group and high dose of inhibitor U0126 treatment group. DBI rat model was established according to the description of Marmarou's diffused brain injury. At 30 min and 1 h, 6 h, 24 h, 48 h and 72 h after injury, morphological changes were observed under light and electronic microscopes. The ERK1/2 phosphorylation and c-Fos were measured by Western blotting. Apoptosis was measured with TUNEL method. Learning and memory function were performed with Morris water maze from 3 days to 7 days after injury. RESULTS: After trauma, some neurons displayed histopathologic changes of necrosis and apoptosis, axon myelin sheath internalization and disconnection. ERK1/2 phosphorylation protein was apparently increased at 30 min after injury, approached peak at 6 h and continued to 24 h. c-fos protein was markedly increased at 30 min after injury, approached peak at 6 h and returned to bottom at 24 h. The number of apoptotic nerve cells increased at 6 h after and approached peak at 72 h. Latencies of searching safety island prolonged. Rats treated with U0126 had reduction in ERK1/2 activity, c-Fos protein, neuronal apoptosis and searching safety island latencies. CONCLUSION: The activated ERK1/2 signaling pathway plays an important role in processing of nerve cell apoptosis after severe DBI.
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Objective To investigate the effect of angiotensin-(1-7) on the expression of cellular c-fos in angiotensin II -induced proliferative glomerular mesangial cells (GMC). Methods GMC were treated with angiotensin II and different dose of angiotensin-(1-7). GMC number were evaluated by crystal violet staining and the expression of c-foe were detected by western blot. Results Angiotensin-(1-7) inhibit angiotensin II -induced GMC proliferation as well as the expression c-foe in a concentration dependent manner. Conclusion c-fos is involved in the inhibiting effects of angiotensin-(1-7) on angiotensin II -induced GMC proliferation.
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AIM:Cinnamyl aldehyde (CA) is one alcohol ingredient derived from Cinnamomum cassia,which is widely used in treating chronic skin wound in Chinese medicine with the curative effect of ‘rescuing YANG’. The purpose of the present study was to investigate the expression of c-Fos, c-Myc proteins at different time points in NIH3T3 treated with CA and explore the possible mechanism of promoting cell proliferation by CA. METHODS: MTT assay was used for observing cell proliferation. Expression of c-Fos and c-Myc proteins in NIH3T3 cells were assessed by immunocytochemistry assay. RESULTS: The cell proliferation was promoted obviously when CA concentration was between 8.8?10-2 ?g/L and 8.8?10 ?g/L. CA at concentration of 5.5 ?g/L significantly induced expression of c-Fos, c-Myc proteins at 2-3 h after the stimulation compared with control group (P
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BACKGROUND: Neuropathic pain produced by nerve injury has the characteristics of enhanced pain responses - allodynia. To understand the pathophysiology of the neuropathic pain, We evaluated the effect of NMDA antagonists and chemical sympathectomy on the c-fos mRNA expression. METHODS: We have divided rats(Sprague-Dawley, N=24) that their left L5 and L6 nerve were tightly ligated into two groups. In NMDA antagonist group(N=17), We injected 10 g MK801 and 10 g 5-amino-phosphonovalerate in three ways, intrathecally before the ligation, after ligation and subcutaneous continuously. Then behavioral tests for mechanical allodynia and cold allodynia were performed. After the test of allodynia,the expression of c-fos were assessed by Northern blot hybridization. In chemical sympathectomy group(N=7), We injected 70 mg/kg guanethidine into the peritoneum in two ways, before the ligation and after ligation. Then same methods were performed in NMDA antagonist group as well. RESULTS: Intrathecal NMDA antagonists before the ligation supressed the elevation of c-fos mRNA expression. Intrathecal NMDA antagonists on the 7 days after the ligation reduced the c-fos mRNA expression and neuropathic pain. Continuous treatment of subcutaneous NMDA antagonists supressed the development of neuropathic pain and the elevation of c-fos mRNA expression. Chemical sympathectomy before the ligation did not supress the elevation of c-fos mRNA expression. Chemical sympathectomy on the 7 days after the ligation reduced neuropathic pain and the elevation of c-fos mRNA expression. CONCLUSIONS: NMDA receptor is related to the induction and maitenance of neuropatic pain, and sympathetic nervous system has a main role in the already induced neuropathic pain.
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Animals , Rats , Blotting, Northern , Dizocilpine Maleate , Guanethidine , Hyperalgesia , Ligation , N-Methylaspartate , Neuralgia , Peritoneum , RNA, Messenger , Sympathectomy , Sympathectomy, Chemical , Sympathetic Nervous SystemABSTRACT
Objective To investigate the expression and co-existence of fos-protein and enkephalin in CNS following enflurane anesthesia. Methods Twelve adult SD rats of both sexes weighing 195-223g were divided randomly into two equal groups: control group and enflurane group: The animals in enflurane group breathed 2% enflurane for 2h. The animals in control group underwent the same experimental steps except enflurane inhalation. Before experiment the animals were kept in a quiet place for 24h and strong light was avoided. After enflurane inhalation, chest was opened and 100 ml of normal saline was infused via left ventricle to wash Out blood from whole body, then followed by infusion of 4% polymerized formaldehyde 0.1mol/L PB 500 ml for fixation of tissue. 90 mm later the whole brain and spinal cord were harvested for determination of fos-protein and enkephalin expression and their location using double-labelled immunohistochemical technique. Results The control group showed more ELI(enkephalin like immunoactivity) neurons, less FLI(fos like immuneactivity) neurons and FLI/ELI(fos and enkephalin like immunoactivity) neurons were very rare. The enflurane group showed more FLI, ELI and FLI/ELI neurons. They were mainly distributed in frontal-cortex, lateral septal nucleus, basolateral amygdaloid nucleus, hippocampus CA1, paraventricular nucleus, ventral posterolateral nucleus, habenular nucleus, ventromedial hypothalamus nucleus, supraoptic nucleus, substantia nigra nucleus, interpeduncular nucleus, periaqueductal gray and dorsal horn. In enflurane group the number of FLI and ELI neurons in these nuclei was significantly higher(P
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AIM: To observe the influence of Ganoderma lucidum spores on the cytokine IL-1? and c-Fos in the brain tissue of epilepsy rats. METHODS: The IL-1? level was examined by radioimmunoassay and the c-Fos expression was measured by immunohistochemical assay. RESULTS: Comparing the Ganoderma lucidum spores group with the epilepsy model group: c-Fos positive cell count in brain cortex and hippocampus in treatment group was obviously reduced. IL-1? level in brain tissue was also reduced obviously. CONCLUSION: Ganoderma lucidum spores effectively reduces cytokine IL-1? in brain tissue of epilepsy rats, improves the immunity dysfunction and plays a role in anti-epilepsy through suppressing c-Fos expression in epilepsy rats brain tissue and blocking of LRG.
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AIM:To investigate the effect of ERK1/2/c-Fos signal pathway during angiotensin-(1-7)inhibiting proliferation of rat glomerular mesangial cell strain(GMCS)induced by angiotensin Ⅱ.METHODS:Rat glomerular mesangial cells(GMC)were co-cultured with angiotensin Ⅱ and different doses of angiotensin-(1-7).The numbers of GMC were evaluated by crystal violet staining.The amounts of p-ERK1/2 and c-Fos expressions were detected by Western blotting.RESULTS:Angiotensin-(1-7)showed its inhibitory effects on GMC number increasing induced by angiotensin Ⅱ as well as the amounts of p-ERK1/2 and c-Fos expressions in a concentration dependent manner.CONCLUSION:ERK/c-Fos signal pathway is involved in the inhibitory effects of angiotensin-(1-7)on angiotensin Ⅱ-induced GMC proliferation.
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AIM: The autoantibodies against ?_1-adrenergic receptor that was found in patients with malignant hypertension, primary hypertension and refractory hypertension has the agonist activity liked the NE, and may play a role in hypertension. In this paper, the effects of this antibody on vascular smooth muscle cell (VSMC) proliferation and its mechanism were to be studied. METHODS: The cultured rat VSMC proliferation induced by the antibodies against ?_1- adrenergic receptor that was purified by the immune affinity chromatography, was measured by the BrdU cell proliferation assay and cell cycle distribution. The expression of c-jun and c-fos were determined by RT-PCR and Western blotting. RESULTS: Compared to the normal IgG, the antibodies against ?_1-adrenergic receptor promoted the VSMC proliferation and increased the mRNA and protein expression of the c-jun significantly. The role was similar to the norepinephrine, and all was blocked by prazosin, while the mRNA and protein expression of c-fos were not affected by the antibodies. CONCLUSION: The antibodies against ?_1-adrenergic receptor promote the rat VSMC proliferation, and increase the expression of c-jun, which maybe play a role in the vascular remodeling in hypertension.