ABSTRACT
Objective:To provide evidence and lay a foundation for quality control and resources utilization of Kochiae Fructus. Method:A total of 23 samples of Kochiae Fructus were collected from the main distribution areas in China. Momordin Ⅰc content was determined via HPLC-ELSD method, and its correlation with growth traits and habitat factors was analyzed using SPSS 23.0 software,as well as the principle component and clustering analysis. Result:Momordin Ⅰc content had a benign linear relationship with HPLC-ELSD peak area within the range between 29.8 mg·L-1 and 178.8 mg·L-1 (R2=0.999 8),with the quantitation limit at 5.79 mg·L-1 and the detection limit at 2.36 mg·L-1. Significant differences (PChinese Pharmacopeia published in 2015.Origin,growth traits,and habitat factors could impact momordin Ⅰc content accumulation in Kochiae Fructus. Moreover,the content had a negative correlation with plant height,stem diameter,leaf length,leaf width,fruit diameter and longitude,and a positive correlation with ratio of length to width of leaves,altitude and latitude. Those from Shanxi,Jilin,and Shandong provinces had a higher momordin Ⅰc content. The characters tested could be simplified to four principle components, and their cumulative contribution rate was 95.831%. Kochiae Fructus samples tested could be divided into four groups,and those from group Ⅰ had superior growth traits, and those from group Ⅲ had higher momordin Ⅰc content. Conclusion:The optimized HPLC-ELSD method for determining momordin Ⅰc content of Kochiae Fructus is convenient,accurate and reproducible,and could be used to control the herbs quality. Those cultivated in a lower longitude,higher altitude,and higher latitude region could accumulate more momordin Ⅰc content. More attention shall be paid to germplasm in Shanxi and Zhejiang with superior resources screening of Kochiae Fructus.
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.