ABSTRACT
Objective:To explore plasma level and activity of endotoxin (LPS)in patients with ischemic stroke (IS). Methods:A total of 80 IS inpatients were regarded as stroke group,and another 50 healthy subjects were treated as healthy control group.Plasma levels of LPS,LPS binding protein (LBP)and sCD14 were measured and compared between healthy control group and IS group on 1d and 3d after stroke.Results:Compared with healthy control group,there were significant rise in plasma levels of LPS,LBP and sCD14 in stroke group on 1d and 3d,P <0.01 all;compared with 1d after stroke,there were significant rise in plasma levels of LPS [(0.29 ±0.07)U/ml vs. (0.38±0.05)U/ml],LBP [(22.13±2.75)μg/ml vs.(27.16±3.75)μg/ml]and sCD14 [(1251.11±179.79)ng/ml vs.(1472.29±158.18)ng/ml]in stroke group on 3d after stroke,P =0.001 all.Conclusion:Plasma level and activity of endotoxin significantly rise in patients with ischemic stroke.It helps clinical physicians to diagnose ische-mic stroke by measuring plasma level and activity of endotoxin.
ABSTRACT
Objective:To explore plasma level and activity of endotoxin (LPS)in patients with ischemic stroke (IS). Methods:A total of 80 IS inpatients were regarded as stroke group,and another 50 healthy subjects were treated as healthy control group.Plasma levels of LPS,LPS binding protein (LBP)and sCD14 were measured and compared between healthy control group and IS group on 1d and 3d after stroke.Results:Compared with healthy control group,there were significant rise in plasma levels of LPS,LBP and sCD14 in stroke group on 1d and 3d,P <0.01 all;compared with 1d after stroke,there were significant rise in plasma levels of LPS [(0.29 ±0.07)U/ml vs. (0.38±0.05)U/ml],LBP [(22.13±2.75)μg/ml vs.(27.16±3.75)μg/ml]and sCD14 [(1251.11±179.79)ng/ml vs.(1472.29±158.18)ng/ml]in stroke group on 3d after stroke,P =0.001 all.Conclusion:Plasma level and activity of endotoxin significantly rise in patients with ischemic stroke.It helps clinical physicians to diagnose ische-mic stroke by measuring plasma level and activity of endotoxin.
ABSTRACT
<p><b>OBJECTIVE</b>To discuss the biological function and regulation mechanism of curcumin in promoting human colorectal carcinoma (LoVo) cells apoptosis.</p><p><b>METHOD</b>Conventional in vitro culture in human colorectal carcinoma cells LoVo, When 80%-90% confluence was reached, cells were treated with curcumin at different concentrations (0-20 mg x L(-1)). Curcumin's effect on cell proliferation level was examined by MTT colorimetry. The ultrastructure of curcumin-treated LoVo cells were observed with transmission electron microscope (TEM). The amount of PI-positive LoVo cells after the curcumin treatment were determined by flow cytometry. The cell apoptosis rate was detected by Annexin V-FITC/PI double staining. The mRNA level of Bax, Bcl-2, Caspase-3 and Bcl-xL were tested by means of RT-PCR.</p><p><b>RESULT</b>MTT test indicates curcumin could inhibite the growth and proliferation of LoVo cells in a time- and concentration-dependent manner. TEM examination showed that curcumin can make LoVo cell morphological changes, showing the typical characteristics of apoptotic cells. Flow cytometry instrument analysis showed that curcumin can arrest cell cycle at S phase, and induce apoptosis of LoVo cells. RT-PCR test showed that curcumin can activate the expression of Bax and Caspase-3, inhibit the expression of Bcl-2 and Bcl-xL at the mRNA level.</p><p><b>CONCLUSION</b>Curcumin can significantly inhibit the proliferation and induce the apoptosis of human colorectal carcinoma cells LoVo. Such biological effect may be associated with activating Caspase-3 signal channel by activating Bax expression and inhibiting Bcl-2 and Bcl-xL expression. This study lays an important foundation for further discussing the mechanism of curcumin in inducing human colorectal carcinoma LoVo apoptosis.</p>