Cervical cancer is one kind of many cancers that cause death to women around the world. Many studies had support the statement that inflammation has a strong linkage with cancer development. Several factors like proinflammatory factor can influence tumor cell microenvironment, and induce a faster proliferation. TNF-α is suspected can induce proliferation. While cancer itself can induce inflammation, which is marked by several marker. One of them is HMGB1, released from the cell as active secretory lysosomes or passive diffusion. Genistein has demonstrated growth inhibitory effects of various types of cancer cells. It inhibits tyrosine kinase pathway, which can be activated by TNF -α. One of those pathways that have the link with proliferation is p38. This study tries to reveal about inhibitory effect of genistein toward p38 pathway that had been activated by TNF-α. This research was conducted by exposing cultured HeLa cells with various doses of genistein for 90 minutes, and then exposed to TNF-α 10 ng / mL for 20 minutes. Observations were made with a confocal microscope, by staining the cells with pp38-TRITC and HMGB1 antibody. The intensity was measured and analyzed by Fluoview software. The results suggest that there be significant differences between pp38 intranuclear intensity and HMGB1 extranuclear intensity of each dose of genistein (p = 0.000, ANOVA). pp38 and HMGB1 intensity were increased along with increasing genistein dose, but at high dose there were noted decreasing of pp38 and HMGB1 intensity. At apoptotic dose, pp38 and HMGB1 intensity w ere increased markedly, showing the effect of apoptosis. In general, increasing doses of genistein increase intranuclear p38 activation and HMGB1 extranuclear translocation. So there were a strong linkage between p38 activation and HMGB1 translocation in this study.
Fatty liver is an accumulation of lipid drops exceeding 5% of the total amount of liver, which can increase the risk of nonalcoholic fatty liver disease (NAFLD). NAFLD is associated with dyslipidemia, which the treatments for both condition are in common. Jati Belanda leaves, Kemuning leaves, Murbei leaves and Bangle rhizome (JKMB) are often used alone or in combination to improve dyslipidemia, but their effect on the liver is unknown.This study used an experimental post test control group method where 25 rats were acclimatized for 2 weeks. After that, the rats were divided into 5 groups including KN : normal feed, KP : DTLM feed, D1 : DTLM+ JKMB extract dose 189 mg/200gbb, D2 : DTLM+ JKMB extract dose 378 mg/200gbb, D3 : DTLM+ JKMB extract dose 756 mg /200gbb and treated for 12 weeks. JKMB extract was obtained in a ratio of 8: 3: 3: 7. After that, the rats were sacrificed and the liver tissue was stained with Hematoxylin-Eosin staining. HE preparations were performed to calculate the percentage of liver fat at 400x magnification with 5 fields of view per slide.The results of the normality (0.200> 0.05) and homogeneity test (0.558> 0.05) were found to be normal. The ANOVA test was found to be significantly different (0.000< 0.05). The Post Hoc test found that the negative control was significantly different from the positive control (0.000 < 0.05). Positive control did not differ significantly with treatment doses D1 (0.094>0.05), D2 (0.186>0.05) and D3 (0.734>0.05).From the results of the research above, it can be concluded that the combination of extracts of Jati Belanda leaves, Kemuning leaves, Murbei leaves and Bangle rhizome extracts could not reduce the percentage of fatty liver.
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