• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.256-263
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• 2007

Background: Intimal hyperpiasia is characterized by a proliferation of vascular smooth muscle cells in the intimal layer Epigallocatechin-3-gallate (EGCG) is known to suppress smooth muscle cell proliferation. We propose that EGCG may have a protective effect against the development of intimal hyperplasia through the suppression of smooth muscle cell proliferation. Material and Method: Human umbilical vein endothelial cells (HUVEC) and rat aortic smooth muscle cells (RASMC) were cultured with different concentrations of EGCG, and proliferation and migration speed were measured. In 20 dogs, the autologous jugular veins were interposed into the carotid arteries. For the study group (n=10), the graft was stored for 30 minutes in EGCG solution and 300mM EGCG was applied to the perivascular space after grafting. After 6 weeks, the intimal and medial thickness was measured. Result: The proliferation of RASMC and HUVEC was suppressed with EGCG. The migration of RASMC was suppressed with EGCG, but that of HUVEC was not affected. In the in vivo study, the intimal thickness was thinner in EGCG group than in the control group (p<0.05), but the medial thickness did not show any difference. The intimal/medial thickness ratio was lower in the EGCG group (p<0.05). Conclusion: EGCG suppresses intimal hyperplasia after vascular grafting, and this may be mediated by prevention of migration and proliferation of vascular smooth muscle cells. The use of EGCG may offer new therapeutic modality to prevent intimal hyperplasia.

• Development and Reproduction
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• v.10 no.2
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• pp.147-154
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• 2006

Phthalates such as di(2-ethyl hexyl)phthalate(DEHP) are industrial chemicals with wide-ranging human exposures because of their use in plastics and other common consumer products. Consequently, their adverse effects as endocrine disruptor in the reproductive physiology of both laboratory rodents and human have been studied extensively. The present study was undertaken to examine whether prepubertal exposure to DEHP affects on the onset of puberty and the associated reproductive parameters such as hormone receptor expressions in female rats. DEHP(100mg/kg/day) was administered daily from postnatal day 25(PND 25) through the day when the first vaginal opening(VO) was observed, and the animals were sacrificed on the next day. Gross anatomy and weight of reproductive tissues were compared to test the DEHP's effects on the cell proliferation. Furthermore, histological studies were performed to assess the structural alterations in the tissues. Specific radioimmunoassay was carried out to measure serum LH levels. To determine the transcriptional changes in progesterone receptor(PR), total RNAs were extracted and applied to the semi-quantitative reverse transcription polymerase chain reaction(RT-PCR). As a result, delayed VO was shown in the DEHP group(PND $37.3{\pm}0.7$) compared to the control group(PND $35.3{\pm}0.7$; p<0.05). DEHP treatment significantly decreased the wet weight of ovaries and uteri compared to the control group(p<0.05). Interestingly, elevation of serum LH levels was shown in the DEHP group(p<0.05). Graafian follicles and corpora lutea were observed only in the ovaries from the control animals. Numerous primary, secondary follicles and small atretic follicles were observed in the ovaries from DEHP-treated animals. Similarly, hypotrophy of luminal and glandular uterine epithelium was found in the DEHP-treated group. These effects were probably due to the inhibitory effects of DEHP on the synthesis and secretion of estrogen from granulosa cells. In the semiquantitative RT-PCR studies, the transcriptional activities of PR in both ovary(p<0.05) and uterus(p<0.01) from DEHP-treated animals were significantly lower than those from the control animals. The present studies demonstrated that the acute exposure to DEHP during the critical period of prepubertal stage could inactivate the reproductive system resulting delayed puberty in female rats.

• Development and Reproduction
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• v.11 no.3
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• pp.245-251
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• 2007

Vinclozolin(VCZ), a systemic dicarboximide fungicide, has been used in the control of diseases caused by microorganism of some species in fruits, vegatables and ornamental plants. Although VCZ itself is a very weak antagonist for androgen receptor binding, both melabolites M1 and M2 are effective antagonists. The present study was undertaken to examine whether prepubertal exposure to VCZ affects on the onset of puberty and the associated reproductive parameters such as hormone receptor expressions in female rats. VCZ(10 mg/kg/day) was administered daily from postnatal day 21(PND 21) through the day when the first vaginal opening(V.O.) was observed. Gross anatomy and weight of reproductive tissues were compared to test the VCZ's effects on the cell proliferation. Furthermore, histological studies were performed to assess the structural alterations in the tissues. To determine the transcriptional changes in progesterone receptor(PR), total RNAs were extracted and applied to the semi-quantitative reverse transcription polymerase chain reaction(RT-PCR). As a result, delayed V.O. was shown in the VCZ group(PND $34.00{\pm}1.22$) compared to the control group(PND $38.20{\pm}1.92$; p<0.01). VCZ treatment significantly decreased the wet weight of ovaries and uteri compared to the control group(p<0.01). Graafian follicles and corpora lutea were observed only in the ovaries from the control animals, while numerous primary, secondary follicles and small atretic follicles were observed in the ovaries from VCZ group. Similarly, hypotrophy of luminal and glandular uterine epithelium was found in the VCZ group. In the semi-quantitative RT-PCR studies, the transcriptional activity of PR in ovary(p<0.01) from VCZ group were significantly lower than those from the control group while in uterus were similar compared with the control group. The present studies demonstrated that the acute exposure to VCZ during the critical period of prepubertal stage could inactivate the reproductive system resulting delayed puberty in female rats.