ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of emodin combined gemcitabine (E&G) on human pancreatic cancer cell line BxPC-3 in vitro.</p><p><b>METHODS</b>BxPC-3 cells were treated with emodin alone in different concentrations (0, 10, 20, 40, 80, and 160 micromol/L, respectively) for 24, 48, and 72 h, and E&G (emodin 40 micromol/L + gemcitabine 20 micromol/L) for 72 h. The inhibition on BxPC-3 cell proliferation was detected by Cell Counting Kit-8 assay and the cell apoptosis of BxPC-3 was determined using flow cytometry.</p><p><b>RESULTS</b>Emodin obviously suppressed the proliferation of BxPC-3 cells in a dose- and time-dependent manner. The survival rates of BxPC-3 cells by 40 micromol/L emodin for 24, 48, and 72 h were 79. 39%, 46. 35%, and 45. 44%, respectively, while the survival rate of BxPC-3 cells acted by 72-h E&G was only 26. 62%, showing significant difference from that by gemcitabine alone (42.78%) and the emodin alone (47.18%). The early apoptotic ratio of BxPC-3 cells induced by 24 h emodin (40 micromol/L) and gemcitabine (20 micromol/L) were 4.70% +/- 1.54% and 11.20% +/- 1.41% respectively, while early apoptotic ratio of BxPC-3 cells induced by E&G was 20.60% +/-3.23%, showing significant difference from that induced by emodin or gemcitabine alone (P<0.05).</p><p><b>CONCLUSIONS</b>Emodin could significantly inhibit BxPC-3 cell growth. It could act synergistically with gemcitabine to inhibit the tumor proliferation of BxPC-3 cells. Its synergistic action was achieved mainly through inducing pancreatic cancer cell apoptosis.</p>
Subject(s)
Humans , Apoptosis , Cell Line, Tumor , Cell Proliferation , Deoxycytidine , Pharmacology , Emodin , Pharmacology , Pancreatic Neoplasms , PathologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of action of emodin for suppressing acute allograft rejection in a rat model of liver transplantation.</p><p><b>METHODS</b>Brown Norway (BW) recipient rats of orthotopic liver transplantation (OLT) were divided into three groups, Group A receiving isografting (with BW rats as donor), Group B receiving allografting (with Lewis rats as donor), Group C receiving allografting and emodin treatment (50 mg/kg daily). They were sacrificed on day 7 of post-transplantation, and their hepatic histology, plasma cytokine levels, and T-cell subset expression were detected.</p><p><b>RESULTS</b>Compared with those in Group A, rats: in Group B exhibited severe allograft rejection with a rejection activity index (RAI) of 7.67+/-0.98, extensive hepatocellular apoptosis with an apoptosis index (AI) of 35.83+/-2.32, and elevated plasma levels of interleukin-2 (IL-2), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-alpha), CD4(+) and CD4 CD4(+)/CD8(+) ratio. However, recipients in Group C showed a decrease in histological grade of rejection and hepatocellular apoptosis, as well as a decrease in plasma levels of IL-2, TNF-alpha, CD4(+) and CD4(+)/CD8(+) ratio, but elevated levels of IL-10 as compared with the allograft group.</p><p><b>CONCLUSION</b>Post-OLT acute rejection could be attenuated by emodin, its mechanism of action may be associated with protecting hepatocytes from apoptosis, polarizing the Th 1 paradigm to Th2, and inhibiting the proliferation of CD4(+) T cell in plasma.</p>