Cigarette smoking affects cyclogeny of spermatogenic cells in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To determine the effects of cigarette smoking on the cyclogeny of spermatogenic cells in rats.</p><p><b>METHODS</b>Rat models of passive smoking were established using a self-made smoking device, and then allocated randomly into two passive smoking groups (A and B, n = 10) and two corresponding control groups (C and D, n = 10). Groups A and B were exposed to cigarette smoke for 8 weeks, followed by the sacrifice of the rats in Groups A and C. And the animals in Groups B and D were killed 48 days after the cessation of passive smoking. The spermatogenesis cycle of each group of rats was detected by flow cytometry, the levels of testosterone (T) and luteinizing hormone (LH) measured by radio-immunity method, and the testis histopathology analyzed by HE staining and transmission electron microscopy.</p><p><b>RESULTS</b>Compared with Group C, Group A showed a significant decrease in the number of spermatids, spermatozoa ([18.76 +/- 3.58]%) and primary spermatocytes ([5.71 +/- 1.18]%) (P < 0.01), but an obvious increase in the spermatogonias ([55.98 +/- 5.35]%, P < 0.01), with a markedly decreased proliferation index ( P < 0.01). The rats of Group A also exhibited pycnosis of spermatocytes, nucleus aberration of Leydig cells, expansion and degranulation of the endoplasmic reticulum, decreased Golgi apparatus, increased lysosomes and fat drops of Sertoli cells, as well as a reduction in the thickness of the wall and the layers of seminiferous tubules and the number of spermatogonia. The T and LH levels were significantly lower in Group A than in C (P < 0.01). After the cessation of passive smoking, a remarkable increase was observed in the percentage of spermatozoa and primary spermatocytes and the levels of serum T and LH in Group B, although the latter were still lower than those of Group D.</p><p><b>CONCLUSION</b>Smoking damages spermatogenic epithelia, Leydig cells and Sertoli cells, reduces the T and LH levels, and block the proliferation of spermatogenetic cells. These changes can be partially reversed after cessation of smoking.</p>

Expressions of voltage-gated K+ channel 2.1 and 2.2 in rat bladder with detrusor hyperreflexia / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Voltage-gated K+ channel (Kv) plays a critical role in the modulation of detrusor contraction. This study was conducted to investigate the expressions of Kv2.1 and Kv2.2 in rat bladder with detrusor hyperreflexia (DH).</p><p><b>METHODS</b>Thirty adult female Sprague-Dawley rats (200-220 g) were randomly divided into the control group and the experimental group. The experimental group was subjected to spinal cord injury (SCI). In the controls, the surgical procedure was identical with the exception that dura and spinal cord were transected. Four weeks after SCI, in vivo cystometry and mechanical pulling tests of isolated detrusor strips were performed. mRNA was extracted from the detrusors of normal and DH rats for the detection of expression of Kv2.1 and Kv2.2 by RT-PCR. Differences in expression between normal and overactive detrusors were identified by gel imaging.</p><p><b>RESULTS</b>Fourteen rats in the experimental group exhibited uninhibited bladder contraction (>8 cmH2O) before voiding after SCI. One rat died from infection. The frequency of DH in the experimental group was significantly different from that in the control group with or without treatment with 4-aminopyridine (4-AP) (P < 0.05), while the amplitude of DH did not change markedly. The rates of variation of the automatic contractile frequency and amplitude were (66.8 +/- 12.4)% and (42.6 +/- 12.6)% respectively in the control group, and (38.4 +/- 9.8)% and (28.0 +/- 4.6)% respectively in the DH group. 4-AP increased the automatic contractile frequency apart from the automatic contractile amplitude in both the control and DH groups (P < 0.05). 4-AP increased the rate of variation of the automatic contractile frequency more markedly in the control group than in the DH group (P < 0.05). Significant expression of Kv2.2 was not detected in bladders in the control group. Compared to the mRNA levels of beta-actin, the mRNA level of Kv2.1 was 1.26 +/- 0.12 in the control group and 0.66 +/- 0.08 in the DH group. SCI significantly reduced the mRNA level of Kv2.1 in rat bladders with DH (P < 0.05).</p><p><b>CONCLUSIONS</b>Our study showed that the mRNA level of Kv2.1 decreased significantly in rat bladder with DH, which was one of the important pathogenetic mechanisms for DH, and suggested that Kv2.1 might be one of the therapeutic targets for bladder overactivity.</p>

Effects of alcohol intake on penile structure and function in rats / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effects of alcohol intake on penile structure and function in rats.</p><p><b>METHODS</b>Thirty adult male Wistar rats were randomly divided into two groups: control group and alcohol intake group. They were administered with 2 mL of normal saline and 40% alcohol solution respectively through gastric tubes every day. Three months later, the animal model of alcohol intake was evaluated by modified Nayagida's method, and the effects of alcohol on the rats were studied by sexual behavior, the number of apomorphine-induced penile erection, level of testosterone in the sera, and the content of penile smooth muscle.</p><p><b>RESULTS</b>The scores of animal model of alcohol intake evaluated by Nayagida's method were 0.66 +/- 2.05 in the control group and 9.26 +/- 5.50 in the alcohol intake group (P < 0.05), which indicated that an animal model of alcohol intake was successfully established. Sexual behavior, the number of apomorphine-induced penile erection, testosterone level in the sera, and the content of penile smooth muscle of the alcohol intake group were all statistically different as compared with the control group (P < 0.05).</p><p><b>CONCLUSION</b>Alcohol intake induces sexual dysfunction in rats, which may be due to the decline of testosterone level in the sera and decline of penile smooth muscle.</p>

The effect of ethanol on sexual function of males and its mechanism / 中华男科学杂志

Though an adequate volume of ethanol relieves nervousness and enhances sexual desire,long term and excessive intake of ethanol can induce sexual dysfunction. The reasons that ethanol results in sexual dysfunction are as follows: ethanol inhibits the hypothalamo-pituitary-testes axis and decreases serum testosterone level. The decline of smooth muscle, choline acetyltransferase and nitric oxide synthase in the penis may be responsible for it.

Relationship between ethanol intake and sexual function in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the relationship between the intake of ethanol and sexual function of rats.</p><p><b>METHODS</b>Sixty adult male Wistar rats were randomly divided into five groups: the control, 10% , 20% , 30% and 40 ethanol groups, which received. . 9% sodium chloride, 10% , 20% , 30% and 40% ethanol solutions respectively at a dose of 2 ml through gastric tubes once a day. Three months later, we observed the effects of ethanol on the sexual function of the rats by their sexual behaviors, the number of apomorphine-induced penile erections, and the content of testosterone in the serum and nitric oxide synthase ( NOS) in the penis.</p><p><b>RESULTS</b>Compared with the control group, the number of apomorphine-induced penile erections in the 10% and 20% ethanol groups was not inhibited significantly (P > 0.05), but the latent period of mounting and intromission in the 10% ethanol group was prolonged and the sexual behaviors in the 20% ethanol group were inhibited except the latent period of ejaculation. The sexual behaviors and the number of apomorphine-induced penile erections of the 30% and 40% ethanol groups were inhibited significantly (P < 0.05). Testosterone in the serum and NOS activity in the penis of the experimental groups were reduced (Pat < 0.05).</p><p><b>CONCLUSION</b>An adequate volume of ethanol does not induce sexual dysfunction in rats, but long term and excessive intake of ethanol may cause penile erectile dysfunction.</p>

The dynamic effects of allogenic transplantations with the bladder acellular matrix grafts of rabbits / 中华外科杂志

<p><b>OBJECTIVE</b>To study the dynamic effects of allogenic transplantations with the bladder acellular matrix grafts (BAMG) of rabbits.</p><p><b>METHODS</b>Hemi-cystectomies were performed in 25 rabbits, and the defects were repaired with BAMG about half bladder size. The rabbits underwent postoperative assessment of bladder function at 8 weeks, including cystometry, vesical volume, vesical compliance and cystography. The allografts were observed by light microscope and electron microscope at 1, 2, 4, 8, 12, 16 weeks after surgery.</p><p><b>RESULTS</b>Macroscopic observation revealed that BAMG regenerated gradually. All urodynamic results of 8 weeks after surgery were not different statistically as compared with these of preoperation (P > 0.05). Cystography revealed that the morphous of bladder was recovered. Epithelialization and neovascularity occurred accompanied by infiltration of inflammatory cell at 1 week. Smooth muscle cell and stratified epithelium regenerated 2 weeks after grafting. Neural elements formed around smooth muscle bundles as early as 4 weeks. Each component regenerated on the frame of BAMG sequentially. After 16 weeks, it was difficult to delineate the junction between the host bladder and BAMG by histology.</p><p><b>CONCLUSION</b>After allogenic transplantation with rabbits' BAMG, the constitution and function of the allografts regenerate completely and gradually on the frame of BAMG.</p>

The roles of protein kinase C and cyclic adenosine monophosphate signal transduction in apoptosis of bladder cancer induced by arsenic trioxide / 中华泌尿外科杂志

Objective To investigate if apoptosis induced by arsenic trioxide(As_2O_3)on bladder cancer T24 cell line is related to the alteration of protein kinase C and cyclic adenosine monophosphate (PKC-cAMP)and its possible mechanism.Methods Apoptosis was studied by TUNEL method.Radio- immunoassay and enzyme immunoassay methods were used to detect the PKC-cAMP alteration in apoptotic process.The expressions and activation of caspase3 were observed by immunocytochemical method and Western blot.Results Atter 24-h drug treatment,the cell apoptosis induced by different concentrations of As_2O_3 was detected by TUNEL method.In control group,the apoptosis rate was 0.86%;PKC level was 2.55 pmol?min~(-1)??g~(-1);cAMP concentration was 22.56 pmol/ml;the expression rate of caspase3 was 8.01%.Compared with control group,the apoptosis rates of 5?mol/L and 10?mol/L As_2O_3 groups increased 8.51-fold and 13.33-fold,respectively;PKC Level decreased 59.22% and 64.71%,respectively;cAMP in- creased 5.34-fold and 4.23-fold,respectively;expression rates of caspase3 increased 3.96-fold and 6.76- fold,respectively.The differences were significant(P＜0.05).Compared with As_2O_3 groups,apoptosis rates of 5?mol/L and 10?mol/L As_2O_3+100nmol/L phorbol 12-myristate 13-aectate(PMA)groups decreased 40.22% and 45.58%,respectively;PKC increased 1.00-fold and 0.76-told,respectively;cAMP decreased 8.37% and 31.46%,respectively;expression rates of caspase3 decreased 51.09% and 65.03%,respective- ly.Activation of caspase3 was detected in As_2O_3-treated groups and As_2O_3+100 nmol/L PMA-treated groups;and activations of caspase3 in PMA-treated groups were weaker than those in As_2O_3-treated groups. Conclusions The antitumor mechanism of As_2O_3 may be the induction of bladder cancer T24 cell apopto- sis by decreasing PKC and increasing cAMP level.