Gentamicin-induced Acute Kidney Injury Research Articles

Attenuative effects of <i>Rosmarinus officinalis</i> on gentamicin-induced acute kidney injury among adult male albino rats

Attenuative effects of <i>Rosmarinus officinalis</i> on gentamicin-induced acute kidney injury among adult male albino rats

Baicalin-2-ethoxyethyl ester alleviates gentamicin-induced acute kidney injury via NF-κB signaling pathway

Drug nephrotoxicity has high fatality rates and complications. To study this conditional, traditionally, Gentamicin (GM) is used to induce acute injury and establish a nephrotic syndrome model. Baicalin, a flavonoid derived from baicalin with potent anti-inflammatory and antioxidant activity, has been used to treat various inflammatory diseases. This study aims to investigate the process of baicalin-2-ethoxyethyl ester (BAE) synthesis and its therapeutic effect on GM-induced acute kidney injury (AKI). Briefly, baicalin was processed by various reactions to yield BAE. A GM-induced AKI model was established for in vivo evaluation of the protective effect and mechanism of BAE. The results indicated that BAE reduced serum creatinine and urea nitrogen levels and improved pathological alterations, inflammatory responses, and oxidative stress in renal tissues. Furthermore, it was revealed that BAE might exert anti-inflammatory and anti-oxidative responses during AKI via the NF-κB signaling pathway regulation. The findings imply that BAE has a protective impact on the kidneys and might serve as a potent medicine for treating renal damage.

Therapeutic Effect of Chitosan-Zinc Oxide Nanoparticles on Acute Kidney Injury Induced by Gentamicin in Wistar Rats

Background: Gentamicin (GM) is an antibiotic frequently used to treat severe gram-negative infections. However, due to nephrotoxicity, its clinical application is restricted. Several lines of evidence indicate that free radicals are important mediators of gentamicin nephrotoxicity. Therefore, the purpose of this research was to examine the potential antioxidant therapeutic value of ZnO-chitosan nanoparticles on gentamicin-induced nephrotoxicity. Methods: Twenty-four rats were divided into four groups (6 rats/group). All groups except group 1 were injected with gentamicin (100 mg/kg body weight i.p.) for eight days. On day 9, rats of groups 1 and 2 were administrated distilled water, and those of groups 3 and 4 were administrated 1/10 and 1/20 LD50 of ZnO-CS-NPs continuously for 30 days. Results: Treatment with ZnO-CS NPs caused a significant decrease in urea, creatinine, uric acid, sodium, potassium, chloride, microalbumin, and malondialdehyde levels; this was accompanied by a significant increase in kidney glutathione reduced, nitric oxide, superoxide dismutase, glutathione S-transferase, and catalase. Conclusion: The findings of the current study revealed that ZnO-CS NP ameliorated kidney injury against gentamicin induced-acute kidney injury in rats by its antioxidant properties.

Protective effect of <i>Rosemarinus officinalis</i> on gentamicin-induced acute kidney injury in adult male albino rats

Background: Gentamicin (GN) drug is one of the first-line drugs for managing severe gramnegative bacteria. Its association with acute kidney injury (AKI) has restricted its use due to oxidation damage to kidney architectural structures. Rosmarinus Officinalis (rosemary) is anatural antioxidant available and affordable in many developing countries. Antioxidants can be used to prevent oxidation that causes AKI in GN use. This study was undertaken to evaluate the protective gross morphological effect of Rosmarinus Officinalis (RO) on Gentamicin- induced acute Kidney injury in male albino rats’ species of Rattus norvegicus.
 Methodology: The study was done in Kenya at Maseno University. A posttest true experimental design was used, and a sample size of 25 Albino rats was calculated using a resource-modified equation. Rats were randomly sampled into 5 groups, each with 5 albino rats. The negative control group received a standard rat diet plus water, the positive control received GN100,mg/kg/bwt/i.p, low-dose RO, medium-dose RO, and high-dose RO groups received 100,150 and 200 mg/kg/bwt of RO orally, respectively, and were co-administered with GN 100mg/kg/bwt/i.p. At the end of day seven, they were humanely sacrificed, and gross morphometric were taken.
 Results: It was observed that the mean weight of the rat, weight, and volume of the kidney increased significantly (p= 0.001) in high-dose RO group as compared to the positive control. The mean length and thickness in high-dose RO group increased significantly (p=0.0001) as compared to the positive control.
 Conclusion: This present study shows that co-administration of a high dose of RO has a protective effect on gross morphology against Gentamicin-induced AKI among male albino rats.

Evaluation of the Utilization of Near-Infrared Fluorescent Contrast Agent ASP5354 for In Vivo Ureteral Identification in Renal Diseases Using Rat Models of Gentamicin-Induced Acute Kidney Injury.

ASP5354 was recently developed as a near-infrared fluorescence (NIRF) contrast agent for intraoperative ureteral identification, and its use has been evaluated in healthy animals. However, the utilization of ASP5354 for ureteral identification has not been evaluated in animals with renal injury. In this study, we assessed the application of ASP5354 for ureteral imaging using rat models of gentamicin-induced mild, moderate, and severe acute kidney injury (AKI), using a clinically available NIRF detection system. NIRF was detected in the abdominal cavity and ureters after laparotomy, and the efficiency of ASP5354 was evaluated based on the NIRF signal intensity over 60 min. After the intravenous injection of ASP5354 into rats with mild or moderate AKI, the ureters were clearly imaged at a high ratio of NIRF intensity in the ureter to that in the tissues around the ureter. Six days after intravenous injection, the use of ASP5354 in rats with moderate AKI did not affect the biochemical kidney functions or histopathological conditions of the kidney tissues, as compared to those with no injection of ASP5354. In rats with severe AKI, ureteral imaging was not effective due to the relatively strong NIRF expression in the tissues around the ureters. These data indicate that ASP5354 holds potential as a contrast agent for intraoperative ureteral identification in patients with limited renal injury.

A new autophagy-driven protective pathway of Haematococcus astaxanthin against chemical damage in wistar rats with gentamicin-induced acute kidney injury

Astaxanthin was established to conserve kidney function and subcellular structure through anti-oxidation and/or the free radical scavenging system, yet little research linked a new protective effect to autophagy or lysosomes. We pre-fed Wistar rats with natural astaxanthin, β-carotene, or placebo and induced acute kidney injury using gentamicin, before examining renal tissues and measuring physiological indices. Qualitative evidence from histopathological and subcellular images, along with quantitative evidence showing treatment effects on blood urea nitrogen and serum creatinine (p < 0.01), indicated that esterified Haematococcus astaxanthin surpassed β-carotene at effectively counteracting chemical damage and protecting the kidneys from injury. Proliferation of enlarged lysosomes and mediation analysis results revealing enhanced lysosomal acid phosphatase activity were consistent with the hypothesized autophagy-lysosomal pathway being up-regulated by astaxanthin intake (p < 0.05). In conclusion, the protective effect of astaxanthin against acute kidney injury exerted through the autophagy-lysosomal detoxification pathway, which totally different from the anti-oxidation and/or conventional SOD-dependent free radical scavenging system, was demonstrated with strong evidence. In light of the pandemic outbreak of novel coronavirus pneumonia associated with a virus preferentially targeting the renal tubular cells, dietary astaxanthin may help bring down incidence rate of coronavirus disease, cases of acute kidney injury secondary to the disease, and mortality rate from acute kidney injury, especially when a standard of care treatment for the infectious disease is pending.

Low nephron endowment increases susceptibility to renal stress and chronic kidney disease.

Preterm birth results in low nephron endowment and increased risk of acute kidney injury (AKI) and chronic kidney disease (CKD). To understand the pathogenesis of AKI and CKD in preterm humans, we generated potentially novel mouse models with a 30%-70% reduction in nephron number by inhibiting or deleting Ret tyrosine kinase in the developing ureteric bud. These mice developed glomerular and tubular hypertrophy, followed by the transition to CKD, recapitulating the renal pathological changes seen in humans born preterm. We injected neonatal mice with gentamicin, a ubiquitous nephrotoxic exposure in preterm infants, and detected more severe proximal tubular injury in mice with low nephron number compared with controls with normal nephron number. Mice with low nephron number had reduced proliferative repair with more rapid development of CKD. Furthermore, mice had more profound inflammation with highly elevated levels of MCP-1 and CXCL10, produced in part by damaged proximal tubules. Our study directly links low nephron endowment with postnatal renal hypertrophy, which in this model is maladaptive and results in CKD. Underdeveloped kidneys are more susceptible to gentamicin-induced AKI, suggesting that AKI in the setting of low nephron number is more severe and further increases the risk of CKD in this vulnerable population.

Liraglutide ameliorates gentamicin-induced acute kidney injury in rats via PGC-1α- mediated mitochondrial biogenesis: Involvement of PKA/CREB and Notch/Hes-1 signaling pathways.

Acute kidney injury (AKI) is a challenging side effect which may clinically impede the use of gentamicin (GM). The present study explored the impact of liraglutide (Lir) on GM-induced kidney injury in rats. Lir (0.2 and 0.4mg/kg, s.c) was given for 10days (a dose/day) starting 3days before giving GM (100mg/kg, i.p) once daily for 7days. Interestingly, Lir notably ameliorated GM-induced elevated levels of renal injury markers; urea and creatinine. Moreover, Lir remarkably mitigated malondialdehyde (MDA) level and elevated glutathione (GSH) level as well as superoxide dismutase (SOD) activity. Also, Lir pre-treatment notably diminished inflammatory markers levels; interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), vascular cell adhesion molecule (VCAM), monocyte chemoattractant protein 1 (MCP-1) and interferon gamma (INF-γ). In addition, Lir significantly replenished expression of Peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1α), Protein kinase A (PKA), cAMP response element-binding protein (CREB), nuclear Nuclear factor erythroid 2-related factor 2 (Nrf2), heme Oxygenase-1 (HO-1), B-cell lymphoma 2 (Bcl-2), and remarkably attenuated expression of Notch homolog 1 (Notch1), Hairy and enhancer of split-1 (Hes-1), Bcl-2-associatedX(Bax), cleaved caspase 3 and nuclear Nuclear factor Kappa B (NF-κB (p65)). The nephroprotective activity of Lir was further confirmed by histopathological examination as well as transmission electron microscopy (TEM). In conclusion Lir achieved its nephroprotective effects through the amelioration of oxidative stress, inflammatory and apoptotic manifestations. It is worth-mentioning that the current study is the first to focus on the involvement of mitochondrial biogenesis and its upstream regulators, PKA/CREB and Notch/Hes-1 signaling pathways in the nephroprotective potentials of Lir. The attenuation of the aforementioned injurious aspects is partially attributed to the improvement of the mitochondrial status as demonstrated by elevated PGC-1α expression via acceleration of PKA/CREB and abatement of Notch/Hes-1 signaling pathways.

Low-intensity pulsed ultrasound (LIPUS) switched macrophage into M2 phenotype and mitigated necroptosis and increased HSP 70 in gentamicin-induced nephrotoxicity

Background and aimMany attempts to control acute kidney injury (AKI) have failed due to a lack of understanding of its pathophysiological key components. Macrophages are a crucial determinant of AKI, which can be categorized functionally as M1 pro-inflammatory and M2 anti-inflammatory macrophages. Low-intensity pulsed ultrasound (LIPUS) is currently being investigated as an immune modulator. The present study aimed to explore the potential effects of LIPUS on the polarization of renal macrophages, as well as the possible interplay between macrophage polarization and necroptosis in gentamicin-induced acute kidney injury. MethodAll rats were randomly allocated into one of four groups: control, LIPUS-treated control, gentamicin acute kidney (GM-AKI), and LIPUS-treated GM-AKI. Renal functions, macrophage polarization, necroptosis, and heat shock protein-70 (HSP70) were analyzed using real-time reverse-transcriptase-polymerase chain reaction (rT-PCR), Western Blot, Enzyme-linked immunosorbent assay (ELISA) as well as immunohistological analysis. Resultswe found that LIPUS markedly inhibited the expressions of M1 macrophage-related genes and promoted significantly the expression of M2 macrophages related genes. This was accompanied by an inhibition of necroptosis and a marked reduction of HSP-70, resulting in a reversal of gentamicin-induced renal alteration. ConclusionFunctional switching of macrophage responses from M1 into M2 seems to be a potential approach to ameliorate necroptosis as well as HSP-70 by low pulsed ultrasound waves in GM-AKI.

The Amomum tsao-ko Essential Oils Inhibited Inflammation and Apoptosis through p38/JNK MAPK Signaling Pathway and Alleviated Gentamicin-Induced Acute Kidney Injury

The clinical application of gentamicin may lead to acute kidney injury (AKI), and the nephrotoxicity of gentamicin is related to the pathological mechanism of several oxidative and inflammatory cytokines. Plant-derived essential oils have good anti-inflammatory and antioxidant properties. This study aimed to clarify the protective effect of Amomum tsao-ko essential oils (AOs) on gentamicin-induced AKI in rats and its possible mechanism. The rat AKI model was induced by intraperitoneal injection of gentamicin. After 14 days of oral AO treatment, the renal function and pathological changes of the kidney tissues were evaluated, and the level of kidney tissue oxidative stress was detected. The content of inflammatory cytokines was measured by ELISA. The expression of ERK1/2, JNK1/2, p38, NF-κB, caspase-3, and Bax/Bcl-2 proteins were estimated by Western blot analysis. The results showed that taking AO reduced the contents of serum urea and creatinine in AKI rats and improve the pathological changes and oxidative stress of the kidney tissue in rats. At the same time, AO reduced inflammation and apoptosis during AKI by regulating the MAPK pathway. The data show that AO has a protective effect on the kidneys and may be a potential drug for treating kidney injury.

Palosuran in Gentamicin-Induced Acute Kidney Injury in an Experimental Rat Model

Palosuran in Gentamicin-Induced Acute Kidney Injury in an Experimental Rat Model

Modulation of gentamicin-induced acute kidney injury by myo-inositol oxygenase via the ROS/ALOX-12/12-HETE/GPR31 signaling pathway.

In this investigation, a potentially novel signaling pathway in gentamicin-induced acute kidney injury—worsened by overexpression of proximal tubular enzyme, myo-inositol oxygenase (MIOX)—was elucidated. WT, MIOX-transgenic (MIOX-Tg), and MIOX-KO mice were used. Gentamicin was administered to induce tubular injury. MIOX-Tg mice had severe tubular lesions associated with increased serum creatinine and proteinuria. Lesions were relatively mild, with no rise in serum creatinine and no albuminuria in MIOX-KO mice. Transfection of HK-2 cells with MIOX-pcDNA led to increased gentamicin-induced reactive oxygen species (ROS). Marked increase of ROS-mediated lipid hydroperoxidation was noted in MIOX-Tg mice, as assessed by 4-HNE staining. This was associated with increased expression of arachidonate 12-lipoxygenase (ALOX-12) and generation of 12-hydroxyeicosatetraenoic acid (12-HETE). In addition, notable monocyte/macrophage influx, upregulation of NF-κB and inflammatory cytokines, and apoptosis was observed in MIOX-Tg mice. Treatment of cells with ALOX-12 siRNA abolished gentamicin-mediated induction of cytokines and 12-HETE generation. HETE-12 treatment promoted this effect, along with upregulation of various signaling kinases and activation of GPCR31. Similarly, treatment of cells or mice with the ALOX-12 inhibitor ML355 attenuated inflammatory response, kinase signaling cascade, and albuminuria. Collectively, these studies highlight a potentially novel mechanism (i.e., the ROS/ALOX-12/12-HETE/GPR31 signaling axis) relevant to gentamicin-induced nephrotoxicity modulated by MIOX.

Exogenous glutathione protects against gentamicin-induced acute kidney injury by inhibiting NF-κB pathway, oxidative stress, and apoptosis and regulating PCNA

This study was designed, for the first time, to examine the possible nephroprotective effects of exogenous glutathione (EGSH) (100 mg/kg, intraperitoneally) on gentamicin-induced acute kidney injury (GM-induced AKI). EGSH reduced renal histopathological changes, inflammatory cell infiltration, and improved renal dysfunction in rats with AKI. EGSH ameliorated GM-induced renal oxidative stress by promoting the renal activities of catalase, glutathione peroxidase, and superoxide dismutase and diminishing renal malondialdehyde and serum nitric oxide levels. Interestingly, EGSH inhibited intrinsic apoptosis by downregulating Bax and caspase-3 and upregulating Bcl2 in the kidney of rats with AKI. EGSH decreased GM-induced inflammatory response as reflected by a remarkable decrease in the protein expressions of NF-κB-p65, IL-6, TNF-α, and iNOS and a considerable diminish in myeloperoxidase activity. Finally, EGSH markedly declined proliferative cell nuclear antigen (PCNA) protein expression in the animals with AKI. In summary, EGSH alleviated AKI in rats intoxicated with GM, partially by inhibiting oxidative stress, NF-κB pathway, and intrinsic apoptosis and regulating PCNA.

Piperazine ferulate attenuates gentamicin-induced acute kidney injury via the NF-κB/NLRP3 pathway

BackgroundPiperazine ferulate (PF) is widely used in chronic nephritis and nephrotic syndrome in clinic. PF can improve diseases related inflammation by inhibiting the activation of nuclear factor kappa-B (NF-κB) signal. Acute kidney injury (AKI) is usually associated with the occurrence and development of renal inflammation. However, the nephroprotective effect and anti-inflammatory mechanisms of PF on AKI are not clear. PurposeThis study aimed to investigate the nephroprotective effects of PF on gentamicin (GM) induced AKI in rats and its potential mechanisms. MethodsMale Sprague Dawley (SD) rats were intraperitoneally injected with GM (100 mg/kg/day) with or without PF (50 and 100 mg/kg/day) for 7 consecutive days. In vitro, the NRK-52e cells were exposed to GM (7 mg/ml) with or without PF (62.5 μg/ml) treatment. The renal injury and cell damage were assessed subsequently. ResultsOur findings showed that PF treatment can significantly improve renal function, reduce renal pathological changes, and attenuate inflammatory response in rats treated with gentamicin. Besides, PF could significantly reduce the cell damage and cellular inflammatory response. In terms of mechanisms, our study revealed that PF can evidently inhibit the activation of NF-κB and nod-like receptor family pyrin domain protein 3 (NLRP3) inflammasome. Meanwhile, it could down regulate the expressions of protein and gene of p-IKKα, p-IKKβ, p-p65, p65, p50, p105, NLRP3 and IL-1β. ConclusionOur findings showed that PF may improve inflammation by inhibiting the NF-κB/NLRP3 pathway, so as to attenuate AKI.

Physalis Alkekengi L. var. Franchetii Calyx Alleviates Gentamicin-Induced Acute Kidney Injury in Rats: Modulation of Oxidative Stress, Inflammation, and Apoptosis

Physalis Alkekengi L. var. Franchetii Calyx Alleviates Gentamicin-Induced Acute Kidney Injury in Rats: Modulation of Oxidative Stress, Inflammation, and Apoptosis

Nephroprotective Activity of Ethanolic Extract of Carissa carandas Leaves against Gentamicin-Induced Acute Kidney Injury in Wistar Albino Rats

The present study was aimed to evaluate the nephroprotective activity of ethanolic extract of Carissa carandas Linn. Leaves (EECC) in Gentamicin-induced nephrotoxicity in Wistar albino rats. The renal damage was induced by Gentamicin (80mg/kg body weight, i.p.). Nephroprotective activity was investigated by the administration of EECC at two different doses (100 and 200mg/kg body weight, p.o) for 28 days and by assessing serum parameters, renal oxidative stress markers and histopathological studies. Gentamicin-treated animals showed an increase in serum creatinine, uric acid, urea, and malondialdehyde (MDA) levels and decrease in total protein, reduced glutathione (GSH), and catalase(CAT) compared to normal control animals, which indicates severe nephrotoxicity. Histopathological studies of kidney Gentamicin-treated animals showed extensive acute tubular necrosis and peri-tubular inflammation. Administration of EECC showed a significant improvement (p&lt;0.05) in biochemical and oxidative stress markers compared to the disease group. EECC treated groups showed better histological appearance when compared to the disease group. Ethanolic extract of Carissa carandas Linn. Leaves showed significant nephroprotective activity against gentamicin-induced acute kidney injury.

Edible Bird Nest Protects the Kidney From Gentamicin Induced Acute Tubular Necrosis.

Every year, there are about 13.3 million cases of acute kidney injury (AKI). Although AKI is a preventable and treatable disease, if left untreated, it has high risk of multiple organ failure and progression to end stage kidney disease. Acute tubular necrosis (ATN) has been recognised as one of the major causes of AKI. Till to date, there is no effective supplement or medication in treating or reversing AKI. Most of the treatment strategies involve preventative measure to minimise the occurrence of AKI or to reverse the cause of AKI. Hence one of the primary area of research interests is to explore the potential treatment for AKI. Edible bird nests (EBN) are edible food produce by the swiftlet’s saliva, which is rich in sialic acids. Sialic acids are monosaccharides that play a vital role in maintaining the integrity and proper function of the human organs, including kidneys. EBN also contains epidermal growth factor, which is widely believed to have rejuvenation and tissue repairing properties. We initiate this study to study the potential reno-protective effect of edible bird’s nests by studying the Wistar rat model of gentamicin-induced AKI. Besides renal profiles, renal histology was also semiquantitatively assessed. In our study, pre-treatment with EBN prevented and ameliorated the gentamicin-induced AKI. To a lesser extent, post-treatment with EBN also protected the kidney from the toxic effect of gentamicin. Our findings are highly indicative that EBN possesses reno-protective properties.

Evaluation of symmetric dimethylarginine and Doppler ultrasonography in the diagnosis of gentamicin-induced acute kidney injury in dogs.

Acute kidney injury is a common problem in dogs and is associated with significant morbidity and mortality. So, the present study aimed to evaluate symmetric dimethylarginine (SDMA) and Doppler ultrasonography including resistive index (RI) in the diagnosis of acute kidney injury in dogs. Ten healthy mongrel dogs were injected with gentamicin sulfate 10% at the dose of 30 mg/kg body weight daily for 10 days for induction of acute kidney injury. Clinical, biochemical, ultrasonographic, and Doppler ultrasonographic examinations and urinalysis were performed for all dogs on 0 day before induction, on the 5th day, and on the 10th day of induction. The results of the current study showed significant increase in plasma level of SDMA, serum urea, creatinine, phosphorus, and potassium and a significant decrease in serum sodium, calcium, and chloride on the 5th day and 10th day of induction, and there was an increase in renal cortical echogenicity of the right and left kidney compared to adjacent liver and spleen, respectively. RI value showed a significant increase on the 5th day and 10th day of induction. The present study showed that SDMA is a sensitive and promising biomarker for diagnosis of acute kidney injury in dogs compared to routine biomarkers; also, the RI of Doppler ultrasonography is useful for early identifying acute kidney injury when the only observable change is an increase in cortical echogenicity.

The Nephroprotective Effect of Zizyphus lotus L. (Desf.) Fruits in a Gentamicin-Induced Acute Kidney Injury Model in Rats: A Biochemical and Histopathological Investigation.

Zizyphus lotus L. (Desf.) (Z. lotus) is a medicinal plant largely distributed all over the Mediterranean basin and is traditionally used by Moroccan people to treat many illnesses, including kidney failure. The nephrotoxicity of gentamicin (GM) has been well documented in humans and animals, although the preventive strategies against it remain to be studied. In this investigation, we explore whether the extract of Zizyphus lotus L. (Desf.) Fruit (ZLF) exhibits a protective effect against renal damage produced by GM. Indeed, twenty-four Wistar rats were separated into four equal groups of six each (♂/♀ = 1). The control group was treated orally with distilled water (10 mL/kg); the GM treated group received distilled water (10 mL/kg) and an intraperitoneal injection of GM (80 mg/kg) 3 h after; and the treated groups received ZLF extract orally at the doses 200 or 400 mg/kg and injected intraperitoneally with the GM. All treatments were given daily for 14 days. At the end of the experiment, the biochemical parameters and the histological observation related the kidney function was explored. ZLF treatment has significantly attenuated the nephrotoxicity induced by the GM. This effect was indicated by its capacity to decrease significantly the serum creatinine, uric acid, urea, alkaline phosphatase, gamma-glutamyl-transpeptidase, albumin, calcium, sodium amounts, water intake, urinary volume, and relative kidney weight. In addition, this effect was also shown by the increase in the creatinine clearance, urinary creatinine, uric acid, and urea levels, weight gain, compared to the rats treated only with the GM. The hemostasis of oxidants/antioxidants has been significantly improved with the treatment of ZLF extract, which was shown by a significant reduction in malondialdehydes levels. Histopathological analysis of renal tissue was correlated with biochemical observation. Chemical analysis by HPLC-DAD showed that the aqueous extract of ZLF is rich in phenolic compounds such as 3-hydroxycinnamic acid, catechin, ferulic acid, gallic acid, hydroxytyrosol, naringenin, p- coumaric Acid, quercetin, rutin, and vanillic acid. In conclusion, ZLF extract improved the nephrotoxicity induced by GM, through the improvement of the biochemical and histological parameters and thus validates its ethnomedicinal use.

Role of Retama Raetam on Gentamicin-Induced Acute Kidney Injury in Experimental Rat Model

The methanol extract of the seeds of Retama raetam was studied for its preventive and curative effects in gentamicin-induced acute renal failure in rats. Twenty-four rats were divided into four different groups. Group 1 was served as a control group, Group 2 and 3 were administered a daily dose of gentamicin (40 mg/kg body weight s.c) for 13 days. In case of group 3, rats were administered with the extract (30 mg/kg b. wt.) from the 14th day onwards for 10 days. While in group 4 rats were treated with an oral dose of the extract equivalent to 30 mg/kg b. wt. after 2 hoursof subcutaneous injection of gentamicin for 13 days. Serum urea and creatinine levels were measured. Moreover, histopathological as well as morphometrical investigations were performed. In the gentamicin model, the methanol extract of R. raetam (30 mg/kg b. wt.) reduced blood urea and serum creatinine effectively in the curative and the preventive treatment. Light microscopic examination of the renal tissues from gentamicin-treated rats revealed severe histopathological and morphometrical changes, whereas specimens obtained from extract-treated rats revealed only mild changes. These findings recommend that the methanol extract of the seeds of R. raetam counteract the deleterious effect of gentamicin on renal tubular function and structure