ABSTRACT
Powder X-ray diffraction (PXRD) technology combined with cluster analysis method was used to classify 75 batches of crystalline ceftriaxone sodium into subtypes, the crystalline characteristics of each subtype were measured with scanning electron microscope (SEM). By comparing some parameters of these subtypes correlated to crystallization process of ceftriaxone sodium, such as salification rate, water content in different subtypes, as well as by studying different lattice stabilities, different compatibilities with rubber closures during accelerated stability tests, the key point to improve the quality of domestic ceftriaxone sodium was disclosed. The results of this paper indicated that the fine structure of the products could be controlled well by improving the salification and crystallization process. As a result, the subtype II of ceftriaxone sodium with high stability can be produced.
ABSTRACT
Objective:To study the molecular mechanism for momordin in inducing apoptosis of multidrug-resistant human chronic leukemia K562/A02 cells. Methods:The growth inhibition value of K562/A02 cells was detected by CCK-8 method. Cell apoptosis was analyzed by Annexin Ⅴ flow cytometry (FCM) and cell morphological examination. FCM was also used in determining expression of P-glycoprotein, p53 protein, bcl-2 protein and caspase activity. Results:Momordin inhibited the proliferation of K562/A02 cells in a dose-dependent manner. It also induced cell apoptosis, reduced the expression of P-glycoprotein, p53 protein and bcl-2 protein, and increased caspase-3 and caspase-8 activity.Conclusion:Momordin reversed the inhibition of apoptosis in multidrug-resistant K562/A02 cells. The molecular mechanism may be related with down-regulation of expression of p53 protein, P-glycoprotein, and bcl-2 protein and up-regulation of caspase-3 and caspase-8 activities.
ABSTRACT
[Objective] To explore effect of momordin on reversion of multidrug resistance(MDR) in K562/A02 cells,and expression and function of P-glycoprotein(P-gp).[Methods] IC50 was detected by CCK-8,and expression of P-gp and retention of ADM in K562/A02 cells were detected by flow cytometry(FCM).[Results] Momordin can improve sensitivity of K562/A02 cells to many kinds of chemotherapeutical drugs,result in decrease of expression of P-gp,and raise concentration of ADM within cells.[Conclusion] Momordin can partly reverse drug resistance of K562/A02 cells,the mechanism of reversion is related with down regulation of expression of P-gp.
ABSTRACT
AIM: To explore the change of the expression of cell adhesion molecule CD_ 54 and CD_ 44 in erythroleukemic K562 apoptosis cells induced by momordin from momordica charantia seeds and study the effects of cell adhesion molecule CD_ 54 and CD_ 44 on cell apoptosis induced by momordin. METHODS: After the treatment of K562 cells with appropriated concentration momordin, CCK-8 test was employed to determine K562 cells growth; flow cytometry FACScan (FITC-Annexin V staining) and electron microscopy were used to detect apoptosis; The expression of CD_ 54 and CD_ 44 were examined by flow cytometry FACScan (FITC-CD_ 54 and PE-CD_ 44 staining). RESULTS: CCK-8 test showed K562 cells growth was significant inhibited by momordin; the apoptosis was detected by cell morphology and flow cytometry FACScan (FITC-Annexin V) in K562 cells after treatment by appropriated concentration momordin. The expressions of CD_ 54 and CD_ 44 in momordin treated K562 cells were 18.62 % and 1.32 % respectively, and in negative momordin treated K562 cells were 0.25 % and 0.17 % respectively, and momordin could up-expresses the protein of CD_ 54 18.37 % and CD_ 44 1.15 %. CONCLUSION: Momordin can markedly induce the K562 cell to apoptosis. The up-expressions of CD_ 54 exist in the process of apoptosis induced by momordin. The change of cell adhesion molecule maybe one of the key factors in the mechanisms of apoptosis induced by momordin, and its mechanism maybe involve in adhesion-dependent apoptosis.
ABSTRACT
Objective: To investigate the effect of Shenmai Injection (Radix Ginseng Rubra, Radix Ophiopogonis) on angiogenesis and the expression of proliferating cell nuclear antigen (PCNA) in tumor tissue, and the mechanism of it in the treatment of tumor. Methods: The mouse tumor model was used to investigate the effect of Shenmai Injection on tumor growth on the whole. The expression of von Willebrand factor (vWF) and PCNA in tumor tissue was studied by means of immunohistochemistry. Results: Shenmai inhibited the tumor growth and reduced microvessel density and the expression of PCNA in tumor tissue. Conclusion:Antiangiogenesis is one of the mechanisms of Shenmai Injection in treatment of tumor.