Please use this identifier to cite or link to this item: http://repository.unmul.ac.id/handle/123456789/4646
Title: Ethyl Acetate Fraction of Kalanchoe pinnata (Lmk)Pers Reduces the Production of IFN-α by Dendritic Cells in Pristane-induced Lupus-like Disease Mice
Authors: Indriyanti, Niken
Keywords: Kalanchoe pinnata, CD123+IFN-α+, lupus, proteinuria, treatment
Issue Date: 2017
Publisher: 7th BASIC-Brawijaya University
Series/Report no.: 2017;
Abstract: IFN-α has a central role in lupus pathogenesis. On the previous study, the ethyl acetate fraction of Kalanchoe pinnata (Lmk) Pers leaves (EF-KP) resulted in the modulation of the T regulatory function and the histology of the kidney. In this study, we observed the effect of the EFKP on the IFN-α secreted by dendritic cells. The model used was Pristane-induced lupus-like disease mice according to Reeves method (2009) [1]. The experimental groups consisted of 3 groups, a positive control group that received placebo, EF-KP group, and negative control group that received cyclophosphamide. The treatment lasted for 3 weeks. At the end of the experiment, the semiquantitative method was used to observe the proteinuria as a general parameter. Then, the dendritic cells were isolated from the femur. The cells were measured by means of flow cytometry method. The proteinuria level of the positive control group was 79,00±33,81 mg/dL. The level of proteinuria of EF-KP group was 42,22±33,36 mg/dL, meanwhile, the negative control group had the level of 36,50±35,59mg/dL. This decrease indicates the repairing effect on of the kidney function. In the IFN-α measurement, we found the relative percentage of CD123+IFN-α+ reduced significantly in the EF-KP and the negative control groups. The result shows the reduction of the relative percentage of CD123+IFN-α+ in the EF-KP group. The decrease is lower than the positive control. It means that the EF-KP is able to inhibit the overexpression of the IFN-α which is produced by the dendritic cells. This inhibition could inhibit the lupus immune-pathogenesis [2], and also the proliferation of the autoreactive B and T cells.
URI: http://repository.unmul.ac.id/handle/123456789/4646
ISSN: 2338-0128
Appears in Collections:A - Pharmacy

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