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【Objective】 To explore the effects of nerve growth factor （NGF） on bladder function and axon injury repair in rats with traumatic spinal cord injury （t-SCI） so as to explore its molecular mechanism. 【Methods】 Traumatic spinal cord injury model was constructed in 30 male SD rats by modified Allen’s beating method. The rats were randomly divided into sham-operation group， injury group and NGF group， with 10 rats in each group. We used the BBB score to observe the motor function of the rats’ hind limbs before and after the operation. The BL-420 biometer experimental system detected the urodynamics. Six anterior roots of the left lumbar taken from the distal end of the anastomosis were stained with toluidine blue， and the number of myelinated axons was counted. We used HE to stain rat bladder tissue， TUNEL to stain the rats’ severely injured spinal cord， and observed the spinal cord apoptosis rate. Western blotting was used to detect the protein expressions of Raf-1， p-MEK-2， MEK-2， ERK1/2， and p-ERK1/2 in spinal cord tissue. 【Results】 The BBB score results showed that there was no difference in the scores of the sham-operation group， the injury group and the NGF group before the operation. After the operation， the scores of the injury group and the NGF group were significantly lower than those in the sham-operation group （P0.05）. 【Conclusion】 NGF may hinder the conduction of MAPK/ERK pathway， thereby affecting the repair of axon damage and improving the bladder function of t-SCI rats.
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Objective To investigate the effect of propofol on the expression of VEGF in Oesophageal carcinoma cells EC9706 and its related molecular mechanism.Methods The expression of VEGF in human Oesophageal carcinoma cells EC9706 and normal esophageal epithelium cells HEEC were compared by immunoblotting.EC9706 was treated with different concentrations of propofol (0,2,6,10μg/L).After incubation,the EC9706 cell lines were detected with MTT,flow cytometry,cell invasion and cell scratch tests.The expression of VEGF,and the phosphorylation of p38 (MAPK) and p44/42 (ERK1/2) were detected by qRT-PCR and immunoblotting in each group.Results The expression of VEGF in EC9706 cells was significantly higher than that in HEEC cells.After propofol intervention,the proliferation,migration and invasion of propofol groups were significantly lower than that of Ctrl group,while the apoptotic rate of propofol groups were significantly higher than that of Ctrl group.The expression of VEGF mRNA and protein in propofol groups were significantly lower than that in Ctrl group.The expression and phosphorylation of p38 (MAPK) and p44 / 42 (ERK1 / 2) were inhibited by propofol.Both of these effects were dose-dependent.Conclusion Propofol inhibits the proliferation,invasion and migration of OC cells EC9706 and promotes apoptosis.Its potential mechanism may work by inhibiting the MAPK/ERK signaling pathway,thereby inhibiting VEGF expression.
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Steroid sulfatase (STS) is an enzyme responsible for the hydrolysis of aryl and alkyl sulfates. STS plays a pivotal role in the regulation of estrogens and androgens that promote the growth of hormone-dependent tumors, such as those of breast or prostate cancer. However, the molecular function of STS in tumor growth is still not clear. To elucidate the role of STS in cancer cell proliferation, we investigated whether STS is able to regulate the integrin signaling pathway. We found that overexpression of STS in HeLa cells increases the protein and mRNA levels of integrin β1 and fibronectin, a ligand of integrin α5β1. Dehydroepiandrosterone (DHEA), one of the main metabolites of STS, also increases mRNA and protein expression of integrin β1 and fibronectin. Further, STS expression and DHEA treatment enhanced phosphorylation of focal adhesion kinase (FAK) at the Tyr 925 residue. Moreover, increased phosphorylation of ERK at Thr 202 and Tyr 204 residues by STS indicates that STS activates the MAPK/ERK pathway. In conclusion, these results suggest that STS expression and DHEA treatment may enhance MAPK/ERK signaling through up-regulation of integrin β1 and activation of FAK.