scholarly journals Protective Effect of Bee Pollen In Acute Kidney Injury, Proteinuria, And Crystalluria Induced By Ethylene Glycol Ingestion In Rats

2021 ◽  
Author(s):  
Asmae Elghouizi ◽  
Noori Al-Waili ◽  
Nawal Elmenyiy ◽  
Salma Elfetri ◽  
Abderrazak Aboulghazi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Ethylene Glycol ◽  
Protective Effect ◽  
Urine Volume ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Histopathological Study ◽  
Pollen Extract ◽  
Bee Pollen ◽  
Antioxidant Content

Abstract Oxidative stress plays a role in hyperoxaluria-induced kidney injury and crystallization. Bee pollen is a hive product with a high content of antioxidants. The antioxidant content and protective effect of bee pollen extract (BPE) against ethylene glycol (EG) induced crystalluria and acute kidney injury (AKI) were investigated. Ten groups of male Wistar rats were treated with EG, cystone (500 mg/kg) or BPE at doses 100, 250, and 500 mg/ kg. On day 30, blood and urine samples were collected for analysis. Kidneys were removed for histopathological study. The antioxidant activity of BPE was assessed, and its total phenols and flavonoids were determined. EG significantly increased urine pH, volume, calcium, phosphorus, uric acid, and protein, and blood urea, creatinine, and liver enzymes (P<0.05). It decreased creatinine clearance and urine magnesium and caused crystalluria. Treatment with BPE or cystone mitigates EG's effect; BPE was more potent than cystone (P<0.05). BPE increases urine volume, sodium, and magnesium compared to the control and EG treated groups. BPE reduces proteinuria and prevents AKI, crystalluria, liver injury, and histopathological changes in the kidney tissue caused by EG. BPE might have a protective effect against EG-induced AKI, crystalluria, and proteinuria, and stone deposition, most likely by its antioxidant content and activity.

DDAH-2 alleviates contrast medium iopromide-induced acute kidney injury through nitric oxide synthase

2019 ◽  
Vol 133 (23) ◽  
pp. 2361-2378 ◽  
Author(s):  
Heng-Huei Lin ◽  
Tzong-Shyuan Lee ◽  
Shing-Jong Lin ◽  
Yi-Chen Yeh ◽  
Tse-Min Lu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Kidney Injury ◽  
Nitric Oxide Synthase ◽  
Protective Effect ◽  
Contrast Medium ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Ros Generation ◽  
Oxide Synthase

Abstract Background: Contrast medium-induced acute kidney injury (CI-AKI) is one of the most common causes of hospital-acquired acute renal failure. However, the pathogenesis of CI-AKI remains unclear. Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor that is largely metabolised by dimethylarginine dimethylaminohydroxylase (DDAH) in humans. Two isoforms of DDAH exist, namely, DDAH-1 and DDAH-2. In the present study, we examined whether the DDAH-2/ADMA/NOS pathway is involved in the pathogenesis of CI-AKI. Methods and Results: Exposure to the contrast medium iopromide led to increase in creatinine and blood urea nitrogen (BUN) levels, accumulation of ADMA, increase in reactive oxygen species (ROS) generation, and an inflammatory response in mice kidney tissue. The injection of adenovirus-harbouring DDAH-2 lowered renal ADMA levels and had a reno-protective effect against contrast-medium injury by decreasing cell apoptosis, ROS, and fibrosis. By contrast, contrast medium-induced renal injury was exacerbated in heterozygous DDAH-2 knockout mice. In the in vitro study, overexpression of DDAH-2 increased the levels of nitrite and intracellular cGMP, while the DDAH-2 knockdown induced the opposite effect. These findings were also observed in the in vivo sample. Conclusions: Our findings provide the first evidence that the DDAH-2/ADMA/NOS pathway is involved in the pathogenesis of CI-AKI and that the protective effect of DDAH-2 probably arises from the modulation of NOS activity, oxidative stress, and the inflammatory process.

Protective effect of Schisandra chinensis bee pollen extract on liver and kidney injury induced by cisplatin in rats

2017 ◽  
Vol 95 ◽  
pp. 1765-1776 ◽  
Author(s):  
Haibo Huang ◽  
Zhenhuang Shen ◽  
Qianqian Geng ◽  
Zhenhong Wu ◽  
Peiying Shi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Kidney Injury ◽  
Pollen Extract ◽  
Schisandra Chinensis ◽  
Bee Pollen ◽  
Liver And Kidney

Roflumilast, a phosphodiesterase 4 inhibitor, attenuates cadmium-induced renal toxicity via modulation of NF-κB activation and induction of NQO1 in rats

2019 ◽  
Vol 38 (5) ◽  
pp. 588-597 ◽  
Author(s):  
MN Ansari ◽  
RI Aloliet ◽  
MA Ganaie ◽  
TH Khan ◽  
Najeeb-ur-Rehman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Urine Volume ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Treated Group ◽  
Renal Tissue ◽  
High Dose ◽  
Dependent Manner ◽  
Histopathological Studies

Objective: In the present study, the protective effect of Roflumilast (ROF, a selective phosphodiesterase (PDE-4) inhibitor) was investigated against cadmium (Cd)-induced nephrotoxicity in rats. Methods: A total of 24 rats were selected and randomly divided into four groups ( n = 6). Group 1 served as the control; groups 2–4 administered with CdCl2 (3 mg/kg, i.p.) for 7 days; groups 3 and 4 were co-administered with ROF in doses of 0.5 and 1.5 mg/kg, orally for 7 consecutive days. Nephrotoxicity was evaluated by measuring urine volume, urea and creatinine levels in urine and serum. Oxidative stress was confirmed by measuring malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) levels in kidney tissue followed by histopathological studies. Results: CdCl2 administration results in a significant ( p < 0.01) decrease in urine volume, urea, and creatinine levels in urine, as well as GSH, SOD, and CAT levels in renal tissue. In addition, Cd also produced significantly increased ( p < 0.01) urea and creatinine levels in serum and TBARS levels in renal tissues. Rats treated with ROF significantly ( p < 0.01) restore the altered levels of kidney injury markers, nonenzymatic antioxidant, as well as depleted enzymes in dose-dependent manner. An increased expression of NF-κB p65 and decreased expression of GST and NQO1 in the Cd only treated group were significantly reversed by high dose of ROF (1.5 mg/kg). Histopathological changes were also ameliorated by ROF administration in Cd-treated groups. Conclusion: In conclusion, ROF treatment showed protective effect against renal damage and increased oxidative stress induced by Cd administration.

scholarly journals Protective effect of glycyrrhizin, a direct HMGB1 inhibitor, on post-contrast acute kidney injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hyewon Oh ◽  
Arom Choi ◽  
Nieun Seo ◽  
Joon Seok Lim ◽  
Je Sung You ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Contrast Media ◽  
Protective Effect ◽  
Inflammatory Cytokines ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Post Contrast ◽  
Pro Inflammatory Cytokines

AbstractPost contrast-acute kidney injury (PC-AKI) is defined as the deterioration of renal function after administration of iodinated contrast media. HMGB1 is known to play an important role in the development of acute kidney injury. The purpose of this study was to investigate the association between HMGB1 and PC-AKI and the protective effect of glycyrrhizin, a direct inhibitor of HMGB1, in rats. Rats were divided into three groups: control, PC-AKI and PC-AKI with glycyrrhizin. Oxidative stress was measured with MDA levels and H2DCFDA fluorescence intensity. The mRNA expressions of pro-inflammatory cytokines (IL-1α, IL-1β, IL-6 and TNF-α) and kidney injury markers (KIM-1, NGAL and IL-18) were assessed using RT-PCR and ELISA in kidney tissue. In addition, the serum and intracellular protein levels of HMGB1were analyzed with the enzyme-linked immunosorbent assay (ELISA) and western blotting. Histologic changes were assessed with H&E staining using the transmission electron microscope (TEM). Moreover, serum creatinine (SCr), blood urea nitrogen (BUN) and lactate dehydrogenase (LDH) levels were assessed. Oxidative stress, pro-inflammatory cytokines, kidney injury markers and LDH were significantly higher in PC-AKI compared to the controls, but were lower in PC-AKI with glycyrrhizin. Intracellular and serum HMGB1 levels significantly increased after contrast media exposure, whereas they markedly decreased after glycyrrhizin pretreatment. SCr and BUN also decreased in PC-AKI with glycyrrhizin compared to PC-AKI. In PC-AKI, we could frequently observe tubular dilatation with H&E staining and cytoplasmic vacuoles on TEM, whereas these findings were attenuated in PC-AKI with glycyrrhizin. Our findings indicate that HMGB1 plays an important role in the development of PC-AKI and that glycyrrhizin has a protective effect against renal injury and dysfunction by inhibiting HMGB1 and reducing oxidative stress.

scholarly journals SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhiya Deng ◽  
Maomao Sun ◽  
Jie Wu ◽  
Haihong Fang ◽  
Shumin Cai ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Cell Model ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Autophagy Induction ◽  
Promising Therapeutic Approach ◽  
Related Proteins ◽  
Caecal Ligation And Puncture

AbstractOur previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.

Protective Effect of Taurine on Mice with Doxorubicin-induced Acute Kidney Injury

2017 ◽  
pp. 1191-1201 ◽  
Author(s):  
Yon-Suk Kim ◽  
Si-Heung Sung ◽  
Yujiao Tang ◽  
Eun-Ju Choi ◽  
Young-Jin Choi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Kidney Injury

scholarly journals Canagliflozin protects against cisplatin-induced acute kidney injury by AMPK-mediated autophagy in renal proximal tubular cells

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Cheol Ho Park ◽  
Bin Lee ◽  
Myeonggil Han ◽  
Woo Joong Rhee ◽  
Man Sup Kwak ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Kidney Injury ◽  
Proximal Tubular Cells ◽  
Cell Viability Assay ◽  
Tubular Cells ◽  
Compound C ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular

AbstractSodium-glucose cotransporter 2 inhibitors, which are recently introduced as glucose-lowering agents, improve cardiovascular and renal outcomes in patients with diabetes mellitus. These drugs also have beneficial effects in various kidney disease models. However, the effect of SGLT2 inhibitors on cisplatin-induced acute kidney injury (AKI) and their mechanism of action need to be elucidated. In this study, we investigated whether canagliflozin protects against cisplatin-induced AKI, depending on adenosine monophosphate-activated protein kinase (AMPK) activation and following induction of autophagy. In the experiments using the HK-2 cell line, cell viability assay and molecular analysis revealed that canagliflozin protected renal proximal tubular cells from cisplatin, whereas addition of chloroquine or compound C abolished the protective effect of canagliflozin. In the mouse model of cisplatin-induced AKI, canagliflozin protected mice from cisplatin-induced AKI. However, treatment with chloroquine or compound C in addition to administration of cisplatin and canagliflozin eliminated the protective effect of canagliflozin. Collectively, these findings indicate that canagliflozin protects against cisplatin-induced AKI by activating AMPK and autophagy in renal proximal tubular cells.

scholarly journals Sepsis Associated Acute Kidney Injury

2021 ◽  
Author(s):  
Titik Setyawati ◽  
Ricky Aditya ◽  
Tinni Trihartini Maskoen
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Fluid Therapy ◽  
Urine Volume ◽  
Kidney Injury ◽  
Rapid Identification ◽  
Hospital Death ◽  
Cell Arrest ◽  
Sepsis And Septic Shock ◽  
Clinical Conditions

AKI is a syndrome consisting of several clinical conditions, due to sudden kidney dysfunction. Sepsis and septic shock are the causes of AKI and are known as Sepsis-Associated AKI (SA-AKI) and accounted for more than 50% of cases of AKI in the ICU, with poor prognosis. Acute Kidney Injury (AKI) is characterized by a sudden decline in kidney function for several hours/day, which results in the accumulation of creatinine, urea and other waste products. The most recent definition was formulated in the Kidney Disease consensus: Improving Global Outcome (KDIGO), published in 2012, where the AKI was established if the patient’s current clinical manifestation met several criteria: an increase in serum creatinine levels ≥0.3 mg/dL (26.5 μmol/L) within 48 hours, an increase in serum creatinine for at least 1.5 times the baseline value within the previous 7 days; or urine volume ≤ 0.5 ml/kg body weight for 6 hours. The AKI pathophysiology includes ischemic vasodilation, endothelial leakage, necrosis in nephrons and microtrombus in capillaries. The management of sepsis associated with AKI consisted of fluid therapy, vasopressors, antibiotics and nephrotoxic substances, Renal Replacement Therapy (RRT) and diuretics. In the analysis of the BEST Kidney trial subgroup, the likelihood of hospital death was 50% higher in AKI sepsis compared to non-sepsis AKI. Understanding of sepsis and endotoxins that can cause SA-AKI is not yet fully known. Some evidence suggests that renal microcirculation hypoperfusion, lack of energy for cells, mitochondrial dysfunction, endothelial injury and cycle cell arrest can cause SA-AKI. Rapid identification of SA-AKI events, antibiotics and appropriate fluid therapy are crucial in the management of SA-AKI.

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