Objective To investigate the effects of β-Carboline of alkaloids on proliferation of SGC-7901 of human gastric cancer cells.Methods SGC-7901 cells were cultured in vitro initially. After SGC-7901 cells were incubated with β-Carboline alkaloids at different concentrations of 5,10, 20,40 μg/mL for 24,48 hours,the inhibited proliferation rate of SGC-7901 cells were examined by Methtl Thiazolyl Tetrazolium(MTT)assay.Morphological changes of SGC-7901 cells were observed by Hoechst 33258 under fluorescence microscope.Flow cytometry was used to detect cell apoptosis after SGC-7901 cells were incubated with β-Carboline alkaloids for 24 hours.Cell gemonic DNA was detec-ted by agarose electrophoresis.Results β-Carboline of alkaloids induced damage of SGC-7901 cell in a concentration dependent manner .The IC 5 0 of β-Carboline alkaloids at 2 4 ,4 8 hours were 17.79 μg/mL and 12.17 μg/mL respectively.Apoptotic cells were observed and flow cytonetry analy-sis in dicated that the apoptosis rate of cells treated with different concentrations of β-Carboline alka-loids(0,5,10,20,40 μg/mL)for 24 and 48 hours were 1.66%,11.27%,20.32%,30.66%, 41.42%;3.84%,15.29%,23.34%,34.87%,49.54%,respectively.Increasing in apoptosis rate of SGC-7901 cells was associated with drug concentration.Typical DNA Ladder was detected in DNA agarose electrophoresis.Conclusion β-Carboline alkaloids can inhibit the proliferation and in-duce the apoptosis of SGC-7901 cells.

Objective To investigate the effects of β-Carboline of alkaloids on proliferation of SGC-7901 of human gastric cancer cells.Methods SGC-7901 cells were cultured in vitro initially. After SGC-7901 cells were incubated with β-Carboline alkaloids at different concentrations of 5,10, 20,40 μg/mL for 24,48 hours,the inhibited proliferation rate of SGC-7901 cells were examined by Methtl Thiazolyl Tetrazolium(MTT)assay.Morphological changes of SGC-7901 cells were observed by Hoechst 33258 under fluorescence microscope.Flow cytometry was used to detect cell apoptosis after SGC-7901 cells were incubated with β-Carboline alkaloids for 24 hours.Cell gemonic DNA was detec-ted by agarose electrophoresis.Results β-Carboline of alkaloids induced damage of SGC-7901 cell in a concentration dependent manner .The IC 5 0 of β-Carboline alkaloids at 2 4 ,4 8 hours were 17.79 μg/mL and 12.17 μg/mL respectively.Apoptotic cells were observed and flow cytonetry analy-sis in dicated that the apoptosis rate of cells treated with different concentrations of β-Carboline alka-loids(0,5,10,20,40 μg/mL)for 24 and 48 hours were 1.66%,11.27%,20.32%,30.66%, 41.42%;3.84%,15.29%,23.34%,34.87%,49.54%,respectively.Increasing in apoptosis rate of SGC-7901 cells was associated with drug concentration.Typical DNA Ladder was detected in DNA agarose electrophoresis.Conclusion β-Carboline alkaloids can inhibit the proliferation and in-duce the apoptosis of SGC-7901 cells.

Objective To explore the mechanism of in myocardial damage due to daunorubicin (DNR)in rats. Methods SD rats were divided into the control group and the DNR group using a random-digital table,each group comprised 15 rats. The rats in the DNR group received intraperitoneal injection of daunorubicin 3. 5 mg/kg once a week for 4 weeks. The rats in the control group received intraperitoneal injection of same volume of 0. 9% sodium chloride solution once a week for 4 weeks. The rats′behavior changes in the 2 groups were observed. The electrocardiographic examination,expression of sarcoplasmic reticulum Ca2﹢-ATP enzyme( SERCA2a)and histopathological test were performed at the end of 1,3 and 4 weeks of the experiment on 5 rats in the 2 groups,respectively. Results The subacute myocardial injury rat model could be reproduced by DNR intraperitoneal injection. The rats in the DNR group developed lassitude,drumble and drowsiness from the second week. The control group rats′activity, body weight and feeding were normal. The electrocardiographic examination in DNR group showed the following results:voltage of QRS wave decreased by more than 30% compared with the normal,ST segment elevation,and P wave peaked. Myocardial tissue histopathological examination revealed turbid cytoplasm, vacuolation,disordered arrangement of muscle fiber,and broadened fiber gaps. The expression of SERCA2a were moderately positive in both groups at the end of the first week. The expression of SERCA2a were weakly positive in the DNR group at the end of the third and fourth weeks. The number of SERCA2a positive cells in the DNR group at the end of the third and fourth weeks was significantly less than that in the control group at the same time points[(42. 2 ± 1. 2)vs(65. 30 ± 1. 6),(35. 2 ± 6. 0)vs(66. 7 ± 1. 5),all P﹤0. 05]. Conclusion DNR may inhibit the expression of SERCA2a in myocardial tissue and it may be one of the mechanisms of DNR′s myocardial toxicity.

Objective To explore the mechanism of in myocardial damage due to daunorubicin (DNR)in rats. Methods SD rats were divided into the control group and the DNR group using a random-digital table,each group comprised 15 rats. The rats in the DNR group received intraperitoneal injection of daunorubicin 3. 5 mg/kg once a week for 4 weeks. The rats in the control group received intraperitoneal injection of same volume of 0. 9% sodium chloride solution once a week for 4 weeks. The rats′behavior changes in the 2 groups were observed. The electrocardiographic examination,expression of sarcoplasmic reticulum Ca2﹢-ATP enzyme( SERCA2a)and histopathological test were performed at the end of 1,3 and 4 weeks of the experiment on 5 rats in the 2 groups,respectively. Results The subacute myocardial injury rat model could be reproduced by DNR intraperitoneal injection. The rats in the DNR group developed lassitude,drumble and drowsiness from the second week. The control group rats′activity, body weight and feeding were normal. The electrocardiographic examination in DNR group showed the following results:voltage of QRS wave decreased by more than 30% compared with the normal,ST segment elevation,and P wave peaked. Myocardial tissue histopathological examination revealed turbid cytoplasm, vacuolation,disordered arrangement of muscle fiber,and broadened fiber gaps. The expression of SERCA2a were moderately positive in both groups at the end of the first week. The expression of SERCA2a were weakly positive in the DNR group at the end of the third and fourth weeks. The number of SERCA2a positive cells in the DNR group at the end of the third and fourth weeks was significantly less than that in the control group at the same time points[(42. 2 ± 1. 2)vs(65. 30 ± 1. 6),(35. 2 ± 6. 0)vs(66. 7 ± 1. 5),all P﹤0. 05]. Conclusion DNR may inhibit the expression of SERCA2a in myocardial tissue and it may be one of the mechanisms of DNR′s myocardial toxicity.

OBJECTIVETo investigate the inhibition role of Kang'ai injection (KAI) in rats with hepatic fibrosis.

METHODAnimal model with liver fibrosis were induced by 0.01% concentration of diethylnitrosamine (DEN). 30 female Wistar rats (160-200 g) were randomly divided into 3 groups: the KAI-DEN group, the DEN group and the blank control group. The KAI-DEN group was administered Kang'ai injection (1 mL x k(-1), intraperitoneal injection, once a week) and the DEN group was administered normal saline intraperitoneal injection. HE staining and VG special staining of liver tissue were used to evaluate liver fibrosis.

RESULTCompared with the DEN group, relatively less structural damage and less pseudolobular formation in the KAI-DEN group. Collagen area of the blank control group, the KAI-DEN group and the DEN group were (6.52 +/- 2.64)% , (17.41 +/- 1.112)% and (20.180 +/- 2.519)% , respectively. The difference was statistically significant, P < 0.05.

CONCLUSIONKang'ai injection could inhibit the formation of DEN-induced liver fibrosis.

Animals ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Humans ; Liver ; drug effects ; pathology ; Liver Cirrhosis ; drug therapy ; pathology ; Male ; Rats ; Rats, Wistar