Protective Effect of MicroRNA-23b on Kidney Injury in Septic Rats Through Regulation of Mothers Against Decapentaplegic Homolog 3 (Smad3)

2021 ◽  
Vol 11 (4) ◽  
pp. 697-703
Author(s):  
Yanlou Bai ◽  
Yuan Liu ◽  
Suwen Jiang
Keyword(s):  
Mesangial Cells ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Kidney Damage ◽  
Beclin 1 ◽  
Control Group ◽  
Glomerular Mesangial Cells ◽  
Model Control ◽  
Smad3 Expression ◽  
Set Up

Our study aims to investigate the mechanism whereby microRNA (miRNA)-23b alleviates kidney damage in septic rats. Herein, we set up septic rat model, control group and sham-operated model to evaluate the kidney tissue damage. The glomerular mesangial cells isolated from rats were transfected with plasmids expressing miR-23b followed by analysis of the expression of miR-23b, Smad3, TLR4, HMGB1 and expression of autophagy-related proteins (LC3, beclin-1) by western blot and RT-qPCR. The level of TNF-α, IL-6 and BUN and SCr were significantly elevated in the model group and decreased after overexpression of miR-23b with elevated LC3-II, Smad3 and Beclin-1 expression. miR-23b mimic group presented highest expression of miR-23b, followed by miR-23b NC group, and miR-23b inhibitor group. The levels of TLR4, and HMGB1 and positive rate of NF-κBp65 in miR-23b mimic group were significantly lower than those in miR-23b inhibitor group (p < 0.05). Importantly, miR-23b has a targeted relationship with Smad3. Overexpression of miR- 23b induces autophagy by promoting the Smad3 expression, alleviates kidney damage in septic rats, and reduces inflammation and inactivates NF-κB signaling pathway.

The Effect of Autophagy Induced by Mothers Against Decapentaplegic Homolog 3 (Smad3) Regulated by MicroRNA (miRNA)-23b on Renal Injury in Septic Rats

2021 ◽  
Vol 11 (9) ◽  
pp. 1825-1831
Author(s):  
Zhao Niu ◽  
Duojiao Fan ◽  
Yang Zhang ◽  
Junling Jiang
Keyword(s):  
Kidney Tissue ◽  
Kidney Damage ◽  
Beclin 1 ◽  
Control Group ◽  
Model Control ◽  
Model Control Group ◽  
Positive Rate ◽  
Smad3 Expression ◽  
Set Up ◽  
Related Proteins

This study intends to investigate the mechanism by how microRNA (miRNA)-23b alleviates kidney damage in septic rats. Herein, septic rat model, control group and sham-operated model were set up to assess kidney tissue damage. Tissues were extracted from the rats and isolated into cells. Then cells were transfected with plasmids expressing miR-23b followed by analysis of the expression of miR-23b, Smad3, TLR4, HMGB1 and autophagy-related proteins (LC3, beclin-1) by western blot and RT-qPCR. The level of TNF-α, IL-6 and BUN and SCr were elevated in the model group and decreased after upregulation of miR-23b with increased LC3-II, Smad3 and Beclin-1 expression. miR-23b mimic group showed highest miR-23b expression followed by miR-23b NC group and miR-23b inhibitor group. The levels of TLR4, and HMGB1 and positive rate of NF-κBp65 in miR-23b mimic group were significantly lower than those in miR-23b inhibitor group (p < 0.05). Importantly, miR-23b directly targeted Smad3 and inhibited its expression. In conclusion, overexpressed miR-23b induces autophagy by promoting Smad3 expression, alleviates kidney damage in septic rats, and reduces inflammation and inactivates NF-κB signaling pathway.

scholarly journals Exploring the Effect of Dapagliflozin on Alcoholic Kidney Injury and Renal Interstitial Fibrosis in Rats Based on TIMP-1/MMP-24 Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yundou Wu ◽  
Peijun Song ◽  
Xinke Yuan ◽  
Dayong Li
Keyword(s):  
Renal Fibrosis ◽  
Interstitial Fibrosis ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Control Group ◽  
Renal Interstitial Fibrosis ◽  
Alcohol Group ◽  
Losartan Group ◽  
Smad3 Expression

Objective. To establish a rat model of alcoholic kidney injury and detect the expression of TIMP-1/MMP-24 in the kidneys of rats with alcoholic kidney injury at the molecular pathological level, so as to explore the mechanism of alcohol abuse leading to kidney injury and renal interstitial fibrosis as well as the alleviation of alcohol-induced kidney injury and inhibition of renal interstitial fibrosis by dapagliflozin. Methods. 48 male rats were randomly divided into 4 groups: control group, alcohol group, alcohol + dapagliflozin group, and alcohol + losartan group, each with 12 rats. Different drugs were administered by gavage for modeling and treatment. Six days later, the rats were sacrificed, blood was collected from the heart to separate the serum, and the blood creatinine (Scr) and urea nitrogen (BUN) contents were detected biochemically. After blood collection, the kidney tissue was taken and fixed in10% neutral formalin. The expression of renal tissue inflammatory factors (CRP, IL-6, and TNF-α) and renal fibrosis indexes (LN, HA, and TGF-β1) were detected; MMP-24 and TIMP-1 in the kidney tissue of rats in different treatment groups were detected, and Smad3 expression was also detected. Results. After treatment, the general condition of the alcohol + dapagliflozin group and the alcohol + losartan group improved to different degrees. The weight first decreased and then gradually increased over time. There was no statistical difference in the weight change between the two groups; Compared with the control group, the Scr level, BUN content, renal index, inflammatory factors, and renal fibrosis indexes in the alcohol group were significantly increased ( P < 0.05 ); after 6 weeks of treatment, in the alcohol + dapagliflozin group and alcohol + losartan group, Scr level, BUN content, kidney index, inflammatory factors, and renal fibrosis indexes were significantly decreased ( P < 0.05 ); the expression of MMP-24 in the kidney tissue of the control group was upregulated, and the expression of TIMP-1 and Smad3 was downregulated; MMP-24 expression was downregulated, and TIMP-1 and Smad3 expression was significantly upregulated ( P < 0.05 ) in the rats of the alcohol group. After dapagliflozin and losartan treatment, MMP-24 expression gradually increased and TIMP-1 and Smad3 expression gradually decreased ( P < 0.05 ). Conclusion. Long-term large-scale alcohol intake can cause kidney tissue damage and fibrotic lesions. The expression of fibrotic cytokines such as TIMP-1 and Smad3 will increase, and the expression of MMP-24 will be decreased. However, dapagliflozin and losartan have certain therapeutic effects on the abovementioned lesions. The mechanism may be downregulating TIMP-1 and Smad3 and upregulating the expression of MMP-24 and other cytokines in the kidney.

scholarly journals Effects of Qijin granules on high glucose-induced proliferation, apoptosis and expression of nuclear factor- κB and MCP-1 in rat glomerular mesangial cells

2021 ◽  
Vol 20 (9) ◽  
pp. 1819-1826
Author(s):  
Yuanfeng Yang ◽  
Gaocai Xiong ◽  
Renhui Yang ◽  
Yuchuan Li ◽  
Yuling Luo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
High Glucose ◽  
Mesangial Cells ◽  
Control Group ◽  
Glomerular Mesangial Cells ◽  
Smad Signaling ◽  
Apoptosis Rate ◽  
Proliferation And Apoptosis ◽  
Protein Expressions ◽  
Tgf Β1

Purpose: To investigate the effects of Qijin granules on high glucose-induced proliferation and apoptosis in rat glomerular mesangial cells (MC).Methods: MC cells from rats were passaged and cultured, and randomly divided into control group (CNG), high glucose group (HGG), Western medicine group (WMG, high glucose + Benazepril + Gliquidone), and Qijin granules 1/2/3 group (high glucose + different doses of Qijin granules). Mesangial cells proliferation was measured using MTT assay. The NF-κB, MCP-1 and inflammatory factors in supernatant were determined by ELISA. Apoptosis rate and cell cycle were assessed by flow cytometry. The apoptosis-related TGF-β1/Smad signaling pathway-related protein expressions were measured by Western blot.Results: The A-value and early apoptosis rate, apoptosis rate and S-phase percentage, and protein expressions of NF-κB, MCP-1, IL-6, IL-2, TNF-ɑ, Bax, Cyt-C, caspase-3, TGF-β1, and p-Smad3 of MC cells in the HGG at 12 h, 24 h and 48 h were higher than those in the CNG. The above indices were lower in the WMG, and Qijin granules 1/2/3 groups than in the HGG. The Bcl-2, Smad7 protein expression level and the percentage of G1 and G2/M phase were lower in the HGG than in the CNG, and the above indeices were higher in the WMG and Qijin granules 1/2/3 group than in HGG.Conclusion: Qijin granules can dose-dependently inhibit high glucose-induced proliferation and apoptosis in rat MC cells, block the cell cycle and reduce inflammatory responses. This may be related to the regulation of NF-κB, MCP-1 and TGF-β1/Smad signaling pathways. These findings provide theoretical and experimental basis for the clinical treatment of early diabetic nephropathy.

scholarly journals Fasudil ameliorated liposaccharide-induced acute kidney injury in mice by inhibiting NLRP3

2021 ◽  
Vol 20 (10) ◽  
pp. 2055-2062
Author(s):  
Xueqian Li ◽  
Chengzhi Zhao
Keyword(s):  
Acute Kidney Injury ◽  
Treatment Group ◽  
Cell Growth ◽  
Mesangial Cells ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Control Group ◽  
Model Group ◽  
Blank Control Group ◽  
Tissue Homogenates

Purpose: To determine the influence of fasudil on LPS-mediated acute kidney injury (AKI) in mice.Methods: Healthy C57 mice (n = 140) of largely similar weight were used in this study. They were assigned to a treatment group (n = 40), a model group (n = 50), and a blank control group (n = 50). Mice in treatment and model groups were injected with lipopolysaccharide (LPS). In the treatment group, each mouse was injected intravenously with fasudil daily before the establishment of the mouse model of AKI. All mice were sacrificed 6 h after establishing the AKI model. Portions of the kidney from mice were used for preparation of tissue homogenates, while the remaining portions were subjected to primary culture. Transformed C3H Mouse Kidney-1 (TCMK1) and mesangial cells from mouse glomeruli (SV40-MES-13) cells were used for assays of cell growth and apoptosis. Blood samples were alsocollected from the mice. Thereafter, the levels of blood urea nitrogen (BUN) and creatinine (Cr) in kidney homogenates of the three groups were determined. Moreover, levels of NLRP3, nuclear factor kappa-B (NF-κB), toll-like receptor 4 (TLR4), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β in the homogenates and blood were assayed. Cell growth and apoptosis were also measured.Results: The treatment group and model group showed higher levels of BUN and Cr than the control group, with a higher level observed in model mice than in the treatment mice. There were significantly higher relative levels of NF-κB, NLRP3 and TLR4 in treatment and model groups than in controls, with a higher level observed in model mice than in treatment mice. There were significantly higher concentrations of inflammatory factors in treatment and model mice groups than in control mice, with higher levels observed in model mice than in treatment mice. The TCMK1 and SV40-MES-13 cells in the two groups showed slower cell growth and stronger apoptosis than those in control group (p < 0.05).Conclusion: Fasudil relieved LPS-mediated AKI in mice by suppressing TLR4/NF-κB signal pathway and lowering NLRP3. Thus, fasudil has potential as a new adjunctive agent for the treatment of AKI.

scholarly journals P1828A PANEL OF URINE BIOMARKERS FOR EARLY KIDNEY INJURY DETECTION IN NEWBORNS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Irina Pevzner ◽  
Kirill Goryunov ◽  
Valentina Vtorushina ◽  
Vasily Popkov ◽  
Denis Silachev ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Urinary Excretion ◽  
Kidney Injury ◽  
Kidney Damage ◽  
Urine Samples ◽  
Reference Level ◽  
Control Group ◽  
Tubular Damage ◽  
Urine Biomarkers ◽  
Rate Of Increase

Abstract Background and Aims Neonatal kidney damage is a wide spread pathology, especially among preterm infants. Acute kidney injury (AKI) in newborns remains one of the most important problems because the features of neonatal nephrogenesis and physiology. The current clinical criteria for the diagnosis of AKI, including pediatric scales pRIFLE and nRIFLE, rely on glomerulal filtration rate (GFR), blood urea nitrogen (BUN), and serum creatinine (SCr), which are the late biomarkers detectable only within days or weeks after kidney damage occurred, and therefore have limitations when used within the first days after birth. Therefore, sensitive and specific tests for early diagnostics of kidney injury are extremely needed in neonatology. Urine biomarkers appear to be promising for early diagnosis of AKI. Quite often renal pathologies result in markedly increased (or decreased) urinary excretion of a number of protein biomarkers, indicating subclinical tubular injury while conventional AKI signs are not manifested yet. The aim of this study was to determine clinical value of urine molecular biomarkers for the prediction of acute kidney injury in newborns. Method Urine samples from newborns with congenital malformation were collected on the 1st day after born, and then once a week until the 21th postnatal day. Urine samples were centrifuged, aliquoted and stored at –80°С until testing. The next urinary biomarkers were analyzed: calbindin 1, clusterin, IL-18, KIM-1, GST-π, MCP-1 and NGAL. Quantitative determination was performed with immunoassay kit Bio-Plex Pro™ RBM Human Kidney Toxicity Panel 1 (Bio-Rad Inc., USA) and Human NGAL ELISA kit (Invitrogen, Germany). Control group included five age-matched healthy infants. Results 8 of 20 patients showed a direct correlation of increased NGAL levels in urine (50-fold compared to control group) with high levels of C-reactive protein in the blood (3-10-fold rise above the reference level). NGAL is the most sensitive marker for assessing AKI or tubular damage. These 8 patients were further investigated for other urine biomarkers. The IL-18 level in urine was slightly increased in 4 patients. IL-18 is proposed to be a predictor for AKI severity and mortality in children with critical illness. KIM-1 has low basal expression in the normal kidney but its appearance is highly specific and sensitive sign for nephrotoxicity in proximal tubules. We observed the increase of KIM-1 urinary excretion for 7 patients. However, we discover the equal occurrence of decrease or increase of urine MCP-1 through studied patients. Elevated levels of urine MCP-1 were earlier observed in experimental maleate induced azotemia, LPS injection and in model of unilateral ureteral obstruction (UUO). An increase of KIM-1 and/or MCP-1 urinary excretion is known to be associated with some risk of AKI development. We found 3-fold growth of urine clusterin in 7 children. It is noticed, that clusterin increased in damaged tubular cells during polycystic kidney disease and renal carcinoma. Additionally, we revealed 7-fold decrease of calbindin 1 in urine of 7 patients. Сalbindin 1 exclusively localized in the kidney distal nephron segment, and its decrease was discribed for models of UUO, glomerulonephritis and cisplatin nephropathy. GST-π protein is found in cells lining the lumen of the distal tubules and is elevated in the urine of patients with sepsis, independently of accompanied AKI. We also observed 10- to 20-fold rising of urine GST-π for all 8 NGAL-positive newborns. Conclusion The specificity, rate of increase, and non-invasive detection of urine markers studied in this work, make them indispensable in clinical practice. However, their use in neonatology is still experimental. We showed potential applicability of wide biomarker panel for early detection and prediction of AKI in newborns.

scholarly journals The Proteasome Inhibitor, MG132, Attenuates Diabetic Nephropathy by Inhibiting SnoN DegradationIn VivoandIn Vitro

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Huang ◽  
Chen Yang ◽  
Qinling Nan ◽  
Chenlin Gao ◽  
Hong Feng ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
High Glucose ◽  
Proteasome Inhibitor ◽  
Kidney Damage ◽  
Control Group ◽  
Glomerular Mesangial Cells ◽  
Proteasome Inhibitor Mg132 ◽  
Ubiquitin Proteasome Pathway ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway

Transforming growth factor-β(TGF-β) has been shown to be involved in diabetic nephropathy (DN). The SnoN protein can regulate TGF-βsignaling through interaction with Smad proteins. Recent studies have shown that SnoN is mainly degraded by the ubiquitin-proteasome pathway. However, the role of SnoN in the regulation of TGF-β/Smad signaling in DN is still unclear. In this study, diabetic rats were randomly divided into a diabetic control group (DC group) and a proteasome inhibitor (MG132) diabetes therapy group (DT group). Kidney damage parameters and the expression of SnoN, Smurf2, and TGF-βwere observed. Simultaneously, we cultured rat glomerular mesangial cells (GMCs) stimulated with high glucose, and SnoN and Arkadia expression were measured. Results demonstrated that 24-hour urine protein, ACR, BUN, and the expression of Smurf2 and TGF-βwere significantly increased (P<0.05), whereas SnoN was significantly decreased in the DC group (P<0.05). However, these changes diminished after treatment with MG132. SnoN expression in GMCs decreased significantly (P<0.05), but Arkadia expression gradually increased due to high glucose stimulation (P<0.05), which could be almost completely reversed by MG132 (P<0.05). The present results support the hypothesis that MG132 may alleviate kidney damage by inhibiting SnoN degradation and TGF-βactivation, suggesting that the ubiquitin-proteasome pathway may become a new therapeutic target for DN.

Study on the Regulation of Compound siRNA Nanoparticles on the Rat Model of Kidney Injury Induced by Sepsis by Inhibiting the Expression of NF-κB and P65

2021 ◽  
Vol 21 (2) ◽  
pp. 1345-1350
Author(s):  
Ye Chen ◽  
Xiaoxia Liu ◽  
Meiling Chen ◽  
Run Yan ◽  
Wenyu Song
Keyword(s):  
Rat Model ◽  
Group Treatment ◽  
Medical Image Analysis ◽  
Intervention Group ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Control Group ◽  
Image Analysis System ◽  
Model Group ◽  
Analysis System

This article explores the pathogenesis of sepsis AKI, and seeks to protect the acute damage of sepsis tissues and organs. This study is to prepare a rat sepsis-induced AKI model by CLP, and to observe the pathological changes of kidney tissue and the function of kidney changes, and observe the effect of siRNA nanoparticles on its intervention, preliminary explore the protective effect and possible mechanism of siRNA nanoparticles on AKI in sepsis rats, and provide more information for the clinical treatment of siRNA nanoparticles in sepsis theoretical and experimental basis. We analysis the benefit and deficiency of nuclear factor-κB (NF-κB) activation in the pathogenesis of glomerulonephritis and its regulatory effect on NF-κB activation. In the rat model group, no treatment was given after injection of nephrotoxic serum, and the rats were sacrificed on the 14th day; the compound siRNA nanoparticle intervention group (treatment group) was given dexamethasone 0.125 daily on the 1st to 14th day after nephrotoxic serum injection. Immunohistochemistry and medical image analysis system were used to observe NF-κB activation of monocyte chemotactic protein-1 (MCP-1) in glomeruli and tubules, and analyze their relationship with proteinuria and glomerular cells. The results showed that the expression of NF-κB in the glomeruli and tubules of the model group was significantly up-regulated regarding to the control group, and MCP-1’s expression in the glomeruli and tubules of the model group was higher than that of the control group. The activation of NF-κB and the expression of MCP-1 in glomeruli are closely related to monocyte infiltration and proteinuria; NF-κB activation and MCP-1 expression in glomeruli and tubules of the compound siRNA nanoparticles intervention group were significantly down-regulated. It was concluded that the activation of NF-κB has great impact on the pathogenesis of glomerulonephritis, and inhibition of NF-κB activation may be one of the mechanisms of anti-nephritis effect.

Antioxidant Research of Persimmon Extraction in Ionizing Radiatio Mice

2011 ◽  
Vol 343-344 ◽  
pp. 1198-1206 ◽  
Author(s):  
Xiang Ning Chen ◽  
Wan Shan Hu ◽  
Yuan Hong Xie ◽  
Yu Hua Li ◽  
Lin Bo Guo ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Good Health ◽  
Control Group ◽  
Group Model ◽  
Dosage Group ◽  
Blank Control Group ◽  
Model Control ◽  
Mda Content ◽  
Set Up

Persimmon has good health function. To further investigate the antioxidant function in vivo, we set up a model mice with ionizing radiation. IRC mice were divided randomly into six groups, Blank control group, Model control group, VE control group, Low dosage group (G1), Middle dosage group (G2) and High dosage group (G3) respectively. Orally given persimmon extract for 35 days, mice were treated with γ-rays. Our results indicated that pervious administration of the persimmon extraction obviously increased the liver index of the mice. And pathological inspection by microscope suggested that orally given persimmon extraction obviously protected the liver cells of the mice. Further analysis demonstrated that persimmon extraction decreased the MDA content, and increased the SOD and GSH-PX activity in both the serum and the liver in the mice after the Ionizing radiation. Our results suggested the protection role of persimmon extraction by inhibiting the oxidation reaction in vivo.

scholarly journals The Effect of Broccoli Extract in Arsenic-Induced Experimental Poisoning on the Hematological, Biochemical, and Electrophoretic Parameters of the Liver and Kidney of Rats

2022 ◽  
Vol 2022 ◽  
pp. 1-9
Author(s):  
Mahdieh Raeeszadeh ◽  
Pouria Karimi ◽  
Nadia Khademi ◽  
Pejman Mortazavi
Keyword(s):  
Heavy Metals ◽  
Blood Cells ◽  
Serum Proteins ◽  
White Blood Cells ◽  
Kidney Tissue ◽  
Kidney Damage ◽  
Control Group ◽  
Histopathological Diagnosis ◽  
Liver And Kidney ◽  
Liver And Kidney Damage

Heavy metals such as arsenic contribute to environmental pollution that can lead to systemic effects in various body organs. Some medicinal plants such as broccoli have been shown to reduce the harmful effects of these heavy metals. The main aim of the present study is to evaluate the effects of broccoli extract on liver and kidney toxicity, considering hematological and biochemical changes. The experimental study was performed in 28 days on 32 male Wistar rats classified into four groups: the control group (C), a group receiving 5 mg/kg oral arsenic (AS), a group receiving 300 mg/kg broccoli (B), and a group receiving arsenic and broccoli combination (AS + B). Finally, blood samples were taken to evaluate the hematological and biochemical parameters of the liver and kidney, as well as serum proteins’ concentration. Liver and kidney tissue were fixed and stained by H&E and used for histopathological diagnosis. The results demonstrated a significant decrease in white blood cells (WBC), red blood cells (RBC), and hemoglobin (Hb) in the AS group compared to other groups. However, in the B group, a significant increase in RBC and WBC was observed compared to the AS and C groups ( P  < 0.05). Moreover, RBC and WBC levels increased significantly in the AS + B group compared to the AS group ( P  = 0.046). However, in the AS group, aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine levels increased, while total protein, albumin, and globulin decreased. This can be a result of liver and kidney damage, which was observed in the AS group. Furthermore, the increase in the concentration of albumin and globulin in the AS + B group was higher than that in the AS group. Infiltration of inflammatory cells and necrosis of the liver and kidney tissue in the pathological evaluation of the AS group were significantly higher than other groups. There was an increase in superoxide dismutases (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC); however, a decrease in malondialdehyde (MDA) concentration was seen in the AS + B group compared to the AS group. It seems that broccoli is highly effective at reducing liver and kidney damage and improving the hematological and biochemical factors in arsenic poisoning conditions.

scholarly journals The Effect of Superoxide Dismutase on Inhibition of Acute Kidney Injury Induced by Sepsis Based on Kidney Tissue Histology and Murine Sepsis Score

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Jufitriani Ismy ◽  
Maimun Syukri ◽  
Dessy R. Emril ◽  
Nanan Sekarwana ◽  
Jufriady Ismy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Superoxide Dismutase ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Male Rats ◽  
Control Group ◽  
Control Group Design ◽  
Group I ◽  
Sepsis Score

Sepsis is one of the leading causes contributing to the incidence of acute kidney injury (AKI). Oxidative stress can be used as the main approach against sepsis-induced AKI. One of the primary antioxidants that plays a role in warding off oxidative stress is superoxide dismutase (SOD). This research aimed to observe the effect of antioxidant SOD in inhibiting sepsis in AKI based on kidney tissue histopathology. The research method was an experimental laboratory with a post-test-only control group design. Twenty-five adult male rats aged 12–16 weeks, weighing between 200 and 250 g, were randomly divided into five groups: Group I, as a positive control, where rats were injected with lipopolysaccharides (LPS); Group II, as a negative control; Group III, as treatment 1, where rats were injected with LPS and administered orally with SOD (Glisodin®) 250 IU daily; Group IV, as treatment 2, where rats were injected with LPS and administered orally with SOD (Glisodin®) 500 IU daily; and Group V, as treatment 2, where rats were injected with LPS and administered orally with SOD (Glisodin®) 1000 IU daily. Rats were administered with SOD (Glisodin®) by oral gavage with a flexible feeding tube for 16 weeks, given once daily in the morning, and then injected with LPS of 10 mg/kg body weight. Glisodin SOD had a significant effect on murine sepsis score (MSS). MSS influenced the tubular injury score linearly. We conclude that the optimal dose of SOD at 1000 IU for inhibiting sepsis-induced AKI incidence is compared to SOD at a dose of 250 and 500 IU. The antioxidant effect of SOD can prevent sepsis-induced AKI with oxidative stress events.

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