Gambaran histopatologik ginjal wistar yang diberi ekstrak binahong pasca pemberian gentamisin

Abstract: Kidney damage can be caused by many things, such as hypovolemia, sepsis, acute glomeluronefritis, rhabdomyolysis and drugs (gentamicin and NSAID). Gentamicin is an broad spectrum antimicrobial with high toxicity. Gentamicin is an aminoglycoside antibiotic known to be toxic to the kidneys and the side effects that gentamicin cause are renal tubular damage. There are many kinds of herbal plant in Indonesia with benefit, one of them is the binahong plants. Binahong (Anredera cordifoli (Ten) Steenis), has a high antioxidant that is equal to 9.614% of the compound flavonoid.5 Antioxidant contained in binahong leaves can be said as nefroprotective on kidney function. This study aims to reveal the renal histopathologic of wistar rat that have administered binahong extract after gentamicin administration. This study was an experimental study using 25 wistar rats that were divided into 5 groups. Group A is the negative control group (terminated the 7th day), while group B, C, D and E (the treatment group) were administered gentamicin 0.3 ml/day for 6 days. After administration of gentamicin, group B immediately terminated (day 7), group C were administered 50 mg/day of binahong extratct for 3 days (terminated on day 10), group D were administered 100 mg/day of binahong extract for 3 days (terminated on day 10), group E were administered gentamicin for 6 days (terminated on day 10). The results showed that the renal histopathological of wistar rats group that were administered gentamicin for 6 days, showed swelling and necrotic tubular epithelial cells. Wistar rats group that were administered of binahong showed regeneration of renal tubular epithelial cells. Conclusion: The administration of Gentamicin with toxical dose or 0.3 ml/day for 6 days showed acute tubular necrosis. Regeneration of renal tubular epithelial cells is better in the group that were administered binahong extract than the group that were administered pellets. Renal histopathologic of wistar rats at administration of binahong extract with dose of 100 mg are better compared to 50 mg. Keywords: gentamicin, binahong extract, histopathologogical image of wistar rat’s kidney Abstrak: Kerusakan ginjal dapat disebabkan oleh berbagai hal, seperti hipovolemia, sepsis, glomeluronefritis akut, rabdomiolisis dan obat-obatan (Gentamisin dan NSAID). Gentamisin tergolong antibiotika (aminoglikosida) yang berspektrum luas dan memiliki toksisitas tinggi. Salah satu efek toksik dari gentamisin adalah menyebabkan kerusakan pada tubulus ginjal. Ada berbagai jenis tanaman herbal di Indonesia yang mempunyai khasiat, salah satunya adalah tanaman binahong, Tanaman binahong (Anredera cordifoli (Ten) Steenis), memiliki antioksidan yang cukup tinggi yaitu sebesar 9,614% senyawa flavonoid. Antioksidan yang terkandung dalam daun binahong dapat dikatakan sebagai nefroprotektif terhadap fungsi ginjal. Penelitian ini bertujuan untuk mengetahui gambaran histopatologik ginjal tikus wistar yang diberi ekstrak binahong pasca pemberian gentamisin. Penelitian ini merupakan penelitian eksperimental yang menggunakan 25 ekor tikus wistar yang dibagi dalam 5 kelompok. Kelompok A merupakan kelompok kontrol negatif (diterminasi pada hari ke-7), sedangkan kelompok B, C, D dan E (kelompok perlakuan) diberi gentamisin 0,3 ml/hari selama 6 hari. Setelah pemberian gentamisin, kelompok B langsung diterminasi (hari ke-7), kelompok C diberi ekstrak binahong 50 mg/hari selama 3 hari (diterminasi pada hari ke-10), kelompok D ekstrak binahong 100 mg/hari selama 3 hari (diterminasi pada hari ke-10). kelompok E diberi gentamisin selama 6 hari (diterminasi pada hari ke-10). Hasil penelitian menunjukkan bahwa kelompok tikus yang diinduksi gentamisin selama 6 hari secara histopatologik memperlihatkan adanya pembengkakan dan nekrosis sel epitel tubulus. Kelompok tikus yang diberi ekstrak binahong menunjukkan regenerasi sel epitel tubulus ginjal Simpulan: Pemberian gentamisin injeksi dosis toksik yaitu 0,3 ml setiap hari selama 6 hari menunjukkan nekrosis tubular akut (NTA). Regenerasi sel epitel tubulus ginjal lebih baik pada kelompok yang diberi ekstrak binahong dibandingkan kelompok yang hanya diberi pelet. Gambaran histopatologik ginjal lebih baik pada pemberian binahong dengan dosis 100 mg dibandingkan dosis 50 mg.Kata kunci: gentamisin, ekstrak binahong, gambaran histopatologik ginjal.

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Knockdown of the Long Noncoding RNA LUCAT1 Inhibits High-Glucose-Induced Epithelial-Mesenchymal Transition through the miR-199a-5p–ZEB1 Axis in Human Renal Tubular Epithelial Cells

BioMed Research International ◽

10.1155/2020/8895003 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

Li-Cai Zhang ◽

Zong-Bin Wei ◽

Shui-Fu Tang

Keyword(s):

Epithelial Cells ◽

High Glucose ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Epithelial Mesenchymal Transition ◽

Negative Control ◽

Tubular Epithelial Cells ◽

Renal Tubular Epithelial Cells ◽

Mesenchymal Transition ◽

Renal Tubular

Renal fibrosis, the leading cause of end-stage renal disease and in which epithelial-mesenchymal transition (EMT) plays a central role, has a complex pathogenesis that is not fully understood. Therefore, we investigated the role of the long noncoding RNA LUCAT1 in the EMT of renal tubular epithelial cells under high-glucose (HG) conditions and the underlying mechanism involved. In this study, we established HG and normal glucose groups of HK-2 cells by treating HK-2 cells 30.0 or 5.5 mmol/L glucose, respectively. To investigate the roles of LUCAT1 and miR-199a-5p in HG-induced EMT, we transfected the HG group with negative control small interfering RNA (siRNA), siRNA targeting LUCAT1, negative control microRNA, or an miR-199a-5p mimic. The results of the quantitative reverse transcription PCR indicated that the LUCAT1 level in the HG group was increased, whereas the miR-199a-5p level was decreased. The EMT in the cells was induced by treatment with HG but was weakened by LUCAT1 knockdown or miR-199a-5p overexpression, which both also inhibited the HG-induced phosphorylation of SMAD3. Moreover, LUCAT1 and ZEB1 mRNA comprised the same microRNA response elements of miR-199a-5p. LUCAT1 knockdown had no effect on the miR-199a-5p level but decreased the HG-induced upregulation of ZEB1. In conclusion, HG conditions induced the upregulation of LUCAT1, and LUCAT1 knockdown inhibited the EMT in HG-treated HK-2 cells. LUCAT1 likely promotes HG-induced EMT through ZEB1 by sponging miR-199a-5p.

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Elimination of etimicin in rat kidneys and alterations of its cytotoxicity to tubular epithelial cells

Human & Experimental Toxicology ◽

10.1177/0960327114550887 ◽

2014 ◽

Vol 34 (5) ◽

pp. 479-486 ◽

Cited By ~ 2

Author(s):

Z-D Li ◽

X-L Zhang ◽

N Yi ◽

F-C Zhang

Keyword(s):

Epithelial Cell ◽

Epithelial Cells ◽

Treated Group ◽

Tubular Epithelial Cell ◽

Control Group ◽

Cell Cytotoxicity ◽

Tubular Epithelial Cells ◽

Renal Tubular Epithelial Cells ◽

Renal Tubular ◽

Rat Kidneys

Etimicin (ETM) can accumulate in kidneys and cause tubular epithelial cell cytotoxicity. This article aims to study ETM elimination in kidneys and its nephrotoxicity, apoptosis, and histopathological insults of renal tubular epithelial cells, after repeated administration. A total of 36 rats were randomly divided into ETM-treated group and vehicle control group. Rats in ETM-treated group were treated intraperitoneally (i.p.) with 100 mg/kg/day ETM and rats in control group received physiological saline (i.p.) for 5 consecutive days. Determination of ETM concentrations accumulated in rat kidneys was carried out by high-performance liquid chromatography on the basis of derivatization with o-phthalaldehyde and by ultraviolet detector. Apoptotic renal tubular epithelial cells were identified by a terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay. Histopathological insults in kidneys were evaluated by hematoxylin and eosin staining. On day 1 after cessation of ETM administration, the accumulation concentration was 347.50 ± 193.30 μg/g tissue; on day 15, ETM concentration became 16.71 ± 9.99 μg/g tissue. Elimination half-life of ETM in rat kidney was about 3.05 days. Apoptotic renal tubular epithelial cells induced by etimicin was recovered gradually from 1544 ± 138 n/mm2 on day 1 to 716 ± 208 n/mm2 on day 15. Histopathological damage was also gradually recovered from vacuolation of tubular epithelial cells as well as renal tubular edema on days 1, 3, and 7 to nearly normal on day 15. From these results, we concluded that renal tubular epithelial cell cytotoxicity induced by ETM can gradually restore with its decreasing concentration in rat kidneys.

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