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Proteinuria Severity in Lupus Nephritis is Associated with Anti-dsDNA Level and Immune Complex Deposit Location in Kidney Engli, Katherina; Handono, Kusworini; Eko, Mudjiwijono Handaru; Susianti, Hani; Gunawan, Atma; Kalim, Handono
Journal of Tropical Life Science Vol 8, No 3 (2018)
Publisher : Journal of Tropical Life Science

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Abstract

Lupus nephritis (LN) is one of the manifestations of Systemic Lupus Erythematosus (SLE), with proteinuria being one of the clinical manifestations. The proteinuria pathogenesis is associated with anti-dsDNA antibody and the location of immune complex deposits within the kidney. This study aims to investigate the correlation of the severity of proteinuria with the location of immune complex deposits and the level of anti-dsDNA antibody in LN. Data were collected in cross-section. Fifty-three patients with LN in Saiful Anwar Hospital Malang, who underwent renal biopsy, were included. Hematoxylin-eosin staining and immunofluorescence analysis were used to assign subjects to different histopathological classes and determine the immune complex deposits. The spot urine samples were evaluated using the dipstick method for semi-quantitative proteinuria. The anti-dsDNA antibody levels were evaluated using the enzyme-linked immunosorbent assay (ELISA). Turbidity and enzymatic tests were conducted to elucidate urine protein and creatinine content, respectively. The level of proteinuria is significantly different among the different locations of immune complex based on the dipstick and protein/creatinine methods (p = 0.021 and p = 0.005, respectively). There was a significant correlation between anti-dsDNA antibody level and the severity of proteinuria (r = 0.326 based on dipstick and r = 0.28 based on protein/creatinine method). Thus, proteinuria in LN is determined by anti-dsDNA level and the location of immune complex deposits in the kidney.
The Effect of Curcumin on Regression of Liver Fibrosis through Decreased Expression of Transforming Growth Factor-β1 (TGF-β1) Supriono, Supriono; Nugraheni, Asri; Kalim, Handono; Eko, Mudjiwijono Handaru
The Indonesian Biomedical Journal Vol 11, No 1 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

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Abstract

BACKGROUND: Transforming growth factor (TGF)-β1 has a pivotal role in liver fibrogenesis. Curcumin effectively prevent the progression of liver fibrosis through inhibition of TGF-β1/Sma and drosophila MAD (Smad) signaling pathway. However, the role of curcumin in the regression of liver fibrosis is still unknown. This study investigated the role of curcumin and TGF-β1 in liver fibrosis regression.METHODS: An experimental Wistar rat model included 6 treatment groups as well as positive and negative control groups. The treatment and positive control groups were injected with carbon tetrachlorid (CCl4) for 9 weeks to induce liver fibrosis. After cessation of injection, 3 of the treatment groups were given curcumin and 3 were given carboxymethylcellulose (CMC) for 2, 5 and 9 weeks, while the positive control was untreated. The negative control was injected with normal saline. TGF-β1 liver tissue levels were analyzed by ELISA, while the TGF-β1 expression in liver cells was analyzed by immunohistochemical assay. The metavir score was used to assess the degree of liver fibrosis. Values of p<0.05 were regarded as statistically significant.RESULTS: Nine weeks of CCl4 injection induced liver fibrosis (metavir F3); and significantly increased TGF-β1 levels and expression in tissues (p=0.00, p=0.021, respectively). Curcumin administration decreased levels and expression of TGF-β1 in the liver and accelerated regression of liver fibrosis. There was a significant correlation between duration of administration of curcumin with an expression of TGF-β1 in the liver tissue (r=0.87; p<0.00).CONCLUSION: Curcumin accelerates regression of liver fibrosis, likely through decreasing of TGF-β1 expression in the liver.KEYWORDS: curcumin, TGF-β1, liver fibrosis regression, CCl4, animal model