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1.
Journal of Pharmaceutical Practice ; (6): 59-64, 2019.
Article in Chinese | WPRIM | ID: wpr-790898

ABSTRACT

Objective To determine the water absorption coefficient of single-flavor root and rhizome Chinese herbal medicine pieces at room temperature, and guide the water addition in the decoction process of decocting machine of Chinese herbal.Methods The water absorption coefficient of 222-flavor root and rhizome Chinese herbal medicine pieces were studied, the simulated prescriptions were decocted according to the recommended formula of the decocting machine manufacturer and the water absorption coefficient, and the amount of liquid were obtained by the two methods which were compared with the amount of liquid required.Results The water absorption coefficients of roots and rhizomes with different textures were quite different.The amount of liquid obtained according to the manufacturer′s recommended formula was quite different from the amount of liquid required and there was no rule to follow.The error of the amount of liquid obtained according to the water absorption coefficient and the amount of liquid required was small and regular.Conclusion The experimental determination of the water absorption coefficient of traditional Chinese medicine decoction pieces could guide the amount of water added to the decoction machine.

2.
China Journal of Chinese Materia Medica ; (24): 2145-2148, 2011.
Article in Chinese | WPRIM | ID: wpr-283239

ABSTRACT

<p><b>OBJECTIVE</b>To study the antiproliferative effects of beta-sitosterul and its mechanism in hepatoma HepG2 cells.</p><p><b>METHOD</b>Cell proliferation was assessed by MTT assay. Cell cycle distribution, apoptosis and mitochondrial membrane potential were measured by high content screening (HCS). The protein expression of caspase-3, caspase-8, caspase-9, Bcl-2, Bax, tBid and cytochrome c in the HepG2 cells were evaluated by Western Blots.</p><p><b>RESULT</b>beta-Sitosterul exerted significant antiproliferative effects in HepG2 cells. Furthermore, beta-sitosterul also induced HepG2 cells apoptosis, lost mitochondrial membrane potential, activated caspase-3, caspase-8 and caspase-9, up-regulate Bax, tBid protein, down-regulation Bcl-2 protein. However, beta-sitosterul had hardly any effects on QSG7701 cells.</p><p><b>CONCLUSION</b>beta-Sitosterul exerted antiproliferative effects and induced HepG2 cells apoptosis via mitochondrial pathway and membrane death receptor pathway.</p>


Subject(s)
Humans , Antineoplastic Agents , Pharmacology , Apoptosis , Apoptosis Regulatory Proteins , Metabolism , Carcinoma, Hepatocellular , Metabolism , Pathology , Cell Cycle , Cell Line, Tumor , Cell Proliferation , Hep G2 Cells , Liver Neoplasms , Metabolism , Pathology , Membrane Potential, Mitochondrial , Sitosterols , Pharmacology
3.
Tumor ; (12): 184-187, 2010.
Article in Chinese | WPRIM | ID: wpr-433298

ABSTRACT

Objective:To elucidate action mechanism of δ-tocotrienol in inducing apoptosis of human hepatoma HepG2 cells. Methods:Cell proliferation and viability were assessed by MTT assay; cell cycle distribution, apoptotic rate and mitochondrial membrane potential were measured by using high content screening system; the expression of apoptosis-related protein such as caspase-3, caspase-8, caspase-9, Bcl-2, Bax, tBid and cytochrome C in the HepG2 cells were evaluated by Western blotting. Results:δ-Toco-trienol inhibited HepG2 cell proliferation and induced apoptosis in a dose-dependent manner. This growth-inhibiting effect of δ-toco-trienol correlated with loss of mitochondrial membrane potential and release of cytochrome C from mitochondria to cytoplasm, and regulation of the protein expression of Bcl-2 family members, such as up-regulation of Bax and tBid and down-regulation of Bcl-2. Subsequently tocotrienol induced the activation of caspase-3, caspase-8, and caspase-9 which finally induced apoptosis of hepatoma HepG2 cells. Conclusion:δ-Tocotrienol induced apoptosis of human hepatoma HepG2 cells via mitochondrial pathway and membrane death receptor pathway.

4.
Chinese Pharmacological Bulletin ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-564381

ABSTRACT

Aim To evaluate the mechanism of HG251-induced apoptosis in K562/DOX cells.Methods Cell viability was assessed by MTT assay;cell cycle distribution,apoptosis and mitochondrial membrane potential were measured by flow cytometry;the protein expressions of P-gp,caspase-3,caspase-8,caspase-9,p53,Bcl-xL and cytochrome c in the K562/DOX cells were evaluated by Western blot.Results HG251 was able to inhibit cells proliferation,induce apoptosis,lose mitochondrial membrane potential,activate caspase-3,caspase-8,caspase-9,up-regulate p53 protein and down-regulate Bcl-xL protein in a dose-dependent manner but it had no effect on P-gp protein expression.Conclusion HG251 could overcome apoptotic resistance via up-regulating p53 protein and down-regulating Bcl-xL protein.In addition,HG251 also induced K562/DOX cells apoptosis via mitochondrial pathway and membrane death receptor pathway.

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