Biomedical subjects

Zhong-cheng Xin

Publications and source records attributed to Zhong-cheng Xin.

4 recordsLinked to original sources

PubMed2006

[Construction of pGEX4T-1-Cox7a2 and expression, purification and identification of the recombinant protein].

OBJECTIVE: To clone and express Cox7a2, one mitochondrial respiratory chain related gene, and to identify its recombinant protein. METHODS: The coding region of Cox7a2 was amplified from primary cultured mouse Leydig cells by RT-PCR. The PCR product was cloned into pGEX4T-1 vector by BamH I and EcoR I sites, and confirmed by DNA sequencing. The recombinant fusion protein vector was transformed and expressed into BL21. The recombinant fusion protein was identified by Western blotting. RESULTS: The entire coding region of Cox7a2 was cloned and expressed. The fusion protein was identified by anti-GST monoclonal antibody using Western blotting. CONCLUSION: The cloning of Cox7a2 and the expression of the recombinant protein would help to study the detailed function of Cox7a2, one respiratory chain related and highly differently expressed gene in the tissues of aging testes.

Animals↗

PubMed2006

[Construction and expression of ATP50 fluorescent protein in TM3 mouse Leydig cells].

OBJECTIVE: To study the expression and localization of ATP50 by construction of ATP50-pEYFP-N1 in primary cultured mouse Leydig cells. METHODS: Primary cultured mouse Leydig cells were confirmed by 3B-HSD staining. ATP50 was cloned into pEYFP-N1 between Bam HI and Eco RI sites. Cell-transfection and living-cell fluorescence imaging microscopy were employed to investigate the sub-cellular localization of YFP-ATP50 in TM3 mouse Leydig cells. RESULTS: ATP50 green fluorescent protein was well co-localized with red fluorescence mitochondrion marker-Mitotracker in TM3 mouse Leydig cells. CONCLUSION: ATP50 was expressed in primary cultured mouse Leydig cells. The fluorescent expression vector of ATP50 was constructed successfully and YFP-ATP50 was located in mitochondria in TM3 mouse Leydig cells, which provided a useful clue for further research on the steroidogenesis dysfunction in aging males.

Adenosine Triphosphatases↗

PubMed2005

[Primary artery erectile dysfunction: one case report].

OBJECTIVE: To evaluate the relationship between the deformation of penile artery and the primary artery erectile dysfunction, and to improve the treatment and diagnosis of primary artery erectile dysfunction. METHODS: One case of primary artery erectile dysfunction was presented with its primary clinic data. RESULTS: The dorsal artery of the penis was thin and the bilateral penile arteries were lacking by arteriography. The implantation of a penile prosthesis significantly improved the patient's erectile function. CONCLUSION: The primary artery erectile dysfunction is a relatively rare disease. The possibility of primary artery erectile dysfunction should be kept in mind. Penile prosthesis implantation is an effective means for the treatment of primary artery erectile dysfunction.

Adult↗

PubMed2004

[Effects of icariin on intracavernosal pressure and systematic arterial blood pressure of rat].

OBJECTIVE: To realize the effect of icariin on erectile function of penis. METHODS: After the cavernous nerve (CN) of rat was isolated unilaterally, the corpora cavernosa (CC) and right carotid artery were exposed. A 26G needle catheter was inserted into the right CC to monitor the intracavernous pressure (ICP), and another 26G needle catheter was inserted into the left CC for drug administration. Another catheter was placed into the carotid artery to monitor mean systematic arterial blood press (MBp). Icariin of different concentrations was administrated intracavernosally, and the ICP and MBp were recorded during electric stimulation on CN. Sildenafil and papaveine were used as controls. The effects of nitric oxide syntheses (NOS) inhibitor N(omega)-nitro-L-arginine (LNNA), and soluble guanylate cyclase inhibitor H-[1,2,4] oxadiazolo [4,3,-a] quinoxalin-1-one (ODQ) on icariin (10(-4)mol/L) induced ICP changes were investigated also. RESULTS: Icariin, sidenafil and papaverine increased the ICP in a dose-depended manner (P < 0.01). Icariin and sildenafil did not influence the MBp (P > 0.05), however, papaverine significant influenced MBp (P < 0.01). EC(50) of Icariin, sildenafil and papaveine on ICP/MBp were 2.23 micro mol/L, 0.24 micro mol/L and 9.73 micro mol/L respectively. ODQ and LNNA significantly decreased ICP induced by icariin (10(-4)mol/L). CONCLUSION: Icariin increases ICP without influence on MBp and such effect is inhibited by LNNA and ODQ significantly. Icariin regulates the activity of NO-cGMP signal pathway on CC to enhance erectile function by oral therapy.

Animals↗