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OBJECTIVE Study the role of estrogen receptor (ER)in the inhibition of cell viability and differentiation induced by bisphenol A (BPA)in micro mass culture of rat e mbryonic midbrain(MB) cells.METHODS Micro mass cultures of MB were prepared fro m rat e mbryonic midbrain on gestation day 13.MB cells were exposed to BPA (10 -4 ,10 -6 ,10 -8 ,10 -10 ,10 -12 mol·L -1 )for 5 d.Cell viability was assessed by neutral red uptake test.MB differentiation was detected by he matoxylin staining and i mage analysis.In order to observe the role of ER pathway in the toxicity induced by BPA,cell cultures were co-treated with ICI182780 0.1 n mol·L -1 ,ta moxifen 1 n mol·L -1 and BPA 0.1 mmol·L -1 for 5 d, the cell viability and foci differentiation were detected.Moreover,the protein expression levels of ER in normal e mbryonic brain of gestation day 18,testis tissue fro m adult rats and midbrain cells untreated with BPA were investigated by Western blot.The mRNA expression levels of ER in normal e mbryonic brain of gestation day 13 and gestation day 18,ovary and testis tissue fro m adult rats,and midbrain cells un-treated with BPA were investigated by real-ti me PCR.The mRNA expression levels of Notch1 and Hes1 in MB cells treated with BPA 0.1 mmol·L -1 were also detected by real-ti me PCR.RESULTS BPA 0.1 mmol·L -1 could inhibited MB cell viability and foci differentiation.However,this effect could not be reversed by ER antagonist.The protein and mRNA expression levels of ER in e mbryonic brain and MB cells untreated with BPA were found to be extre mly low.In addition,BPA 0.1 mmol·L -1 could inhibited the mRNA expression levels of Notch1 and Hes1 .CONCLUSION BPA could inhibited MB cell viability and foci differentiation.ER pathway might be not involved in this effect.Instead,Notch-Hes pathway might be involved for this effect.
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Objective: To investigate the direct protective effect of SiniTang (SNT) on cultured myocardial cells of neonatal rats injuried by hypoxia and reoxygenation. Methods: The contracting frequency and content of primary-cultured myocardial cells sampled from different groups (control, oxygen and glucose deprivation model, and theated groups with 8. 0, 17. 9, 40, 89. 4, 200?g/mL SNT) were determined by TV recording system and computer image analysis system at different time (hypoxia for 30min, 60min, 90min, 120min, 150min, 180min and reoxygenation for 30min, 60min). The LDH activity in culture media was measured colorimetrically. The quantity of surviving myocardial cells was measured with MTT reduction method. Results: The contraction frequency and range of cultured myocardial cells decreased during hypoxia, the myocardial cells'pulsation of the groups treated with SNT was kept longer than the oxygen and glucose deprivation model, and the myocardial cells treated with SNT of 200?g/mL pulsed again after reoxygenation. After hypoxia for 3 hours, the LDH release of oxygen and glucose deprivation model was significant higher than that of the control ( P
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<p><b>OBJECTIVE</b>To study the immunotoxicity induced by 9,10-dimethyl-1,2-benzathrancene (DMBA) in metallothionein gene-knocked-out mice [MT(-/-)] as compared with that in wild-type mice [(MT(+/+)].</p><p><b>METHODS</b>Female mice were treated with 25 mg/kg and 50 mg/kg of DMBA i.p., respectively and immunized with sheep red blood cells (SRBC) i.v. on the following day and rechallenged by injection of SRBC via footpad s.c. on the fourth day post-immunization. Humoral and cell-mediated immune function was assessed by the number of spleen IgM antibody plaque formation cells (PFC) to SRBC and cell-mediated delayed-type hypersensitivity (DTH) measured by footpad swelling thickness.</p><p><b>RESULTS</b>After treatment with 25 mg/kg DMBA, a decrease in weight of their spleen and thymus and PFC/spleen were observed in MT(-/-) mice, while only decrease in thymus weight of MT(+/+) mice. The humoral function was suppressed by 72% in MT(-/-) mice. No obvious change in cell-mediated immune function was observed both in MT(-/-) and MT(+/+) mice. Both humoral and cell-mediated immune function were suppressed more severe (91%) in MT(-/-) mice treated with 50 mg/kg DMBA than those treated with 25 mg/kg DMBA (72%). DTH was not altered by DMBA in MT(+/+) mice. The weight of their spleen and thymus decreased and humoral immune function suppressed in MT(+/+) mice, but these changes were significantly less severe. No obvious suppression of cell-mediated immune function was observed in MT(+/+) mice.</p><p><b>CONCLUSION</b>Their humoral and cell-mediated immune function was more susceptible to being suppressed by DMBA in MT(-/-) mice, indicating that MT could protect their immune function from damage caused by DMBA.</p>