Abstract:Objective:
To evaluate the renoprotective effects of berberine and/or pentoxifylline in reduction of diclofenac-induced acute kidney injury (AKI) in rats.
Material and Methods:
Fifty male Sprague-Dawley rats were allocated into five groups, Group 1: Rats treated with distilled water plus normal saline for 12 days. Group 2: Rats treated with distilled water plus diclofenac for 12 days. Group 3: Rats treated with berberine plus diclofenac for 12 days. Group 4: Rats treate… Show more
“…These histopathological changes were correlated with the elevated KIM-1, NGAL, MDA, and reduced SOD, GSH sera levels as confirmed by different studies. [27]…”
BACKGROUND: The renin–angiotensin system (RAS) is essential in renal physiology; however, disturbance of the RAS is one of the chief pathways involved in renal injury. Dysregulation of RAS may result in both glomerular and tubulointerstitial injuries through direct effects of angiotensin II (Ang II) type 1 receptor. Irbesartan and other Ang II blockers have renoprotective effect through reduction of on renal inflammations. Therefore, the aim of the present study was to demonstrate the renoprotective effect of irbesartan on gentamicin-induced nephrotoxicity in rats concerning the oxidative stress.
MATERIALS AND METHODS: Thirty Sprague-Dawley Male rats divided into three groups, Group I (10 rats) treated with distilled water, Group II (10 rats) treated with gentamicin, and Group III (10 rats) treated with gentamicin plus irbesartan for 12 days. Blood urea, serum creatinine, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione reductase (GSH), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecules (KIM-1), and cystatin-c were measured in each group.
RESULTS: Irbesartan significantly reduced blood urea, serum creatinine, serum MDA, NGAL, KIM-1, and cystatin-c P < 0.05. Irbesartan significantly increases SOD P < 0.05 without significant effect in elevation of GSH serum levels.
CONCLUSION: Irbesartan has renoprotective effect in attenuation of acute nephrotoxicity through modulation of oxidative stress and antioxidant capacity in rats.
“…These histopathological changes were correlated with the elevated KIM-1, NGAL, MDA, and reduced SOD, GSH sera levels as confirmed by different studies. [27]…”
BACKGROUND: The renin–angiotensin system (RAS) is essential in renal physiology; however, disturbance of the RAS is one of the chief pathways involved in renal injury. Dysregulation of RAS may result in both glomerular and tubulointerstitial injuries through direct effects of angiotensin II (Ang II) type 1 receptor. Irbesartan and other Ang II blockers have renoprotective effect through reduction of on renal inflammations. Therefore, the aim of the present study was to demonstrate the renoprotective effect of irbesartan on gentamicin-induced nephrotoxicity in rats concerning the oxidative stress.
MATERIALS AND METHODS: Thirty Sprague-Dawley Male rats divided into three groups, Group I (10 rats) treated with distilled water, Group II (10 rats) treated with gentamicin, and Group III (10 rats) treated with gentamicin plus irbesartan for 12 days. Blood urea, serum creatinine, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione reductase (GSH), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecules (KIM-1), and cystatin-c were measured in each group.
RESULTS: Irbesartan significantly reduced blood urea, serum creatinine, serum MDA, NGAL, KIM-1, and cystatin-c P < 0.05. Irbesartan significantly increases SOD P < 0.05 without significant effect in elevation of GSH serum levels.
CONCLUSION: Irbesartan has renoprotective effect in attenuation of acute nephrotoxicity through modulation of oxidative stress and antioxidant capacity in rats.
“…Kim-1 and NGAL are more specific for predicting AKI since they are tested in different types of AKI and larger clinical studies, allowing earlier detection of kidney injury before an increase in SCr and/or BUN and before the initiation of renal proximal tubules damages. Accordingly, we can monitor the effects of an intervention or treatment ( 46 ).…”
Background: Acute kidney injury (AKI), also known as acute renal failure (ARF), has received considerable critical attention in recent years. Gentamicin (GM) is an antibiotic whose prolonged use results in AKI with a high mortality rate.Methods: Fifty adult female albino rats weighing 150–200 g were used. The animals were divided into five groups: the first group was the normal healthy control one, the second group received only 1 × 106 HUCB mononuclear cells (MNCs)/rat by intravenous (iv) injection, the third diseased group was given GM 100 mg/kg for 10 consecutive days by intraperitoneal injections, the fourth preventive group received 1 × 106 HUCB MNCs/rat by iv injection 24 h before gentamicin treatment, and the fifth treated group received 1 × 106 HUCB MNCs/rat by iv injection 24 h after gentamicin treatment. After 1 week of treatment, blood samples were collected, and kidneys were removed for histopathological examination.Results: Rats treated with HUCB MNCs in the treated group had a significant decrease in renal damage, low levels of biomarkers for nephrotoxicities such as serum creatinine and blood urea nitrogen, and low chromosomal aberrations compared to the diseased third group. The gene expression of KIM-1 and NGAL was decreased in response to HUCB treatment.Conclusions: HUCB MNCs have a curative effect against AKI and gentamicin-induced genotoxicity owing to their regenerative property.
Objective:
To evaluate the nephroprotective effect of lycopene (LPN) in acute kidney injury (AKI) regarding the oxidative stress (OS).
Materials and Methods:
Thirty Sprague Dawley male rats were divided into three groups – control group: rats treated with distilled water (orally) for 10 days (
n
= 10); AKI group: rats treated with distilled water and diclofenac (intraperitoneal) for 10 days (
n
= 10); treated group: rats treated with LPN (orally) and diclofenac for 10 days (
n
= 10). Body mass index (BMI) and estimated glomerular filtration rate (eGFR) were measured. Blood urea, serum creatinine (CreSerum), serum malondialdehyde (MDA), superoxide dismutase (SOD), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecules (KIM-1) were measured in the all groups on the 11
th
day of the experiment.
Results:
Diclofenac-induced AKI led to significant elevations of BMI, CreSerum, and blood urea compared with control (
P
< 0.05). In AKI model, eGFR was reduced to 11.69 ± 2.64 ml/min/1.73 compared with control group (15.88 ± 3.75 ml/min/1.73,
P
= 0.03). NGAL, MDA, and KIM-1 were elevated in AKI compared with control (
P
< 0.001). Pretreatment with LPN led to the reduction of blood urea and CreSerum as compared with AKI (
P
< 0.001). Similarly, eGFR was increased significantly to 14.81 ± 3.21 ml/min/1.73 compared with 11.69 ± 2.64 ml/min/1.73 in AKI (
P
= 0.02). Serum levels of NGAL, KIM-1, and MDA were reduced significantly in the LPN group as compared with AKI (
P
= 0.001), while the SOD serum level was increased to 33. 86 ± 8.61 pg/ml as compared to 22.78 ± 7.56 pg/ml in AKI (
P
= 0.006). As well, LPN reduced MDA/SOD ratio as compared with AKI (
P
= 0.00001).
Conclusion:
The finding of this study illustrated that LPN is an effective natural antioxidant that attenuates and prevents AKI through modulation of OS and lipid peroxidation. As well, LPN might be of great value in the prevention of nephrotoxicity that induced by nephrotoxic agents like diclofenac.
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