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1.
National Journal of Andrology ; (12): 267-270, 2017.
Article in Chinese | WPRIM | ID: wpr-812774

ABSTRACT

Gap junctions (GJ), as a special membrane structure between adjacent cells, are composed of connexins (Cx) and regulate the proliferation and differentiation of cells. Studies show that gap junctional intercellular communication is weakened or lost in most tumor cells and this abnormality is often accompanied by changed expression of Cxs. Cx43 is a major connexin in the testis tissue. This review focuses on the latest progress in the studies of Cx43 in testicular tumors.


Subject(s)
Animals , Male , Cell Communication , Cell Differentiation , Connexin 43 , Metabolism , Gap Junctions , Metabolism , Testicular Neoplasms , Metabolism
2.
National Journal of Andrology ; (12): 400-404, 2014.
Article in Chinese | WPRIM | ID: wpr-309700

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of total flavonoids of Litsea Coreana (TFLC) on the gap junction (GJ) intercellular communication in TM3 testicular Leydig cells and whether TFLC can reduce the cytotoxicity of oxaliplatin (OHP) in vitro.</p><p><b>METHODS</b>We detected the effect of TFLC on the dye spread of the in vitro cultured TM3 cells by parachute assay, observed changes in the expression of connexin 43 (Cx43) total protein in the TFLC-treated TM3 cells by Western blot, and determined the effects of TFLC on the expression of Cx43 on the membrane of the TM3 cells by immunofluorescence assay and on the cytotoxicity of OHP by MTT assay.</p><p><b>RESULTS</b>TFLC obviously enhanced the GJ function with the increasing of the TFLC concentration in the TM3 cells. Western blot and immunofluorescence assay confirmed that TFLC significantly enhanced the expression of Cx43 total protein and Cx43 expression on the membrane of the TM3 cells. MTT assay showed that at a high cell density (confluent with GJ formation), 20 microg/ml TFLC enhanced the GJ function of the TM3 cells and reduced the cytotoxicity of OHP (P < 0.05), while at a low density (preconfluent with no GJ formation), TFLC exhibited no effect on the cytotoxicity of OHP (P > 0.05).</p><p><b>CONCLUSION</b>TFLC increases the Cx43 expression and GJ function in normal TM3 Leydig cells, and the enhancement of GJ function reduces the cytotoxicity of OHP.</p>


Subject(s)
Humans , Male , Antineoplastic Agents , Toxicity , Cell Communication , Physiology , Cell Count , Connexin 43 , Metabolism , Flavonoids , Pharmacology , Gap Junctions , In Vitro Techniques , Leydig Cells , Litsea , Chemistry , Organoplatinum Compounds , Toxicity , Proteins , Metabolism
3.
Chinese Journal of Hepatology ; (12): 451-454, 2009.
Article in Chinese | WPRIM | ID: wpr-310062

ABSTRACT

<p><b>OBJECTIVES</b>To investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1beta.</p><p><b>METHODS</b>The proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expression and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen I were detected by the quantitative immunocytochemical assay and ELISA.</p><p><b>RESULTS</b>Danshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-1beta (P < 0.05). Synthesis and secretion of Type I collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1beta was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu.</p><p><b>CONCLUSION</b>Danshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type I collagen, possibly via the repression of the JNK signal transduction.</p>


Subject(s)
Animals , Male , Rats , Blotting, Western , Cell Proliferation , Cells, Cultured , Collagen Type I , Metabolism , Bodily Secretions , Dose-Response Relationship, Drug , Down-Regulation , Hepatic Stellate Cells , Metabolism , Immunohistochemistry , Interleukin-1beta , Pharmacology , JNK Mitogen-Activated Protein Kinases , Metabolism , Lactates , Pharmacology , Liver Cirrhosis , Mitogen-Activated Protein Kinases , Metabolism , Rats, Wistar , Signal Transduction
4.
Journal of Southern Medical University ; (12): 914-921, 2009.
Article in Chinese | WPRIM | ID: wpr-268812

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the inhibitory effect of danshensu on c-Jun N-terminal kinase (JNK) and nuclear factor-kappa B (NF-kappaB) signaling in activated rat hepatic stellate cells (HSCs) and explore the mechanisms of danshensu for inhibiting hepatic fibrosis.</p><p><b>METHODS</b>MTT colorimetric assay was used to detect the proliferation of rat HSCs treated with danshensu, and the apoptosis of the cells was analyzed with Annexin- V-FITC/PI and AO/EB staining. The expressions of P-IkappaB-alpha, NF-kappaBP65 and JNK in HSCs stimulated by IL-1beta with subsequent danshensu treatment were observed by Western blotting. Type III collagen in the medium of HSCs was detected by ELISA and immunocytochemistry.</p><p><b>RESULTS AND CONCLUSIONS</b>Danshensu inhibited the activation and proliferation of HSCs, and increased the apoptotic rate of HSCs and reduced the synthesis and secretion of type III collagen. Danshensu showed obvious inhibitory effect on JNK and P-IkappaB-alpha phosphorylation and NF-kappaBP65 expression in HSCs stimulated by IL-1beta. The mechanism of the actions of dansgensu may be mediated by inhibition of JNK and NF-kappaB signal transduction.</p>


Subject(s)
Animals , Male , Rats , Down-Regulation , Hepatic Stellate Cells , Cell Biology , Metabolism , Interleukin-1beta , Pharmacology , Lactates , Pharmacology , MAP Kinase Kinase 4 , Metabolism , Rats, Wistar , Signal Transduction , Transcription Factor RelA , Metabolism
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