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

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.