Anti-oxidant impact of Lisinopril and Enalapril against acute kidney injury induced by doxorubicin in male Wistar rats: involvement of kidney injury molecule-1

Asaad, Gihan F.; Hassan, Azza; Mostafa, Rasha E.

doi:10.1016/j.heliyon.2021.e05985

Cited by 26 publications

(20 citation statements)

References 34 publications

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“…The immune reactivity was visualized by using diaminobenzidine (DAB; Sigma Chemical Co., USA). Immunohistochemical expression of COX2 and NF-kꞵ in the hepatic tissues was semi-quantitatively assessed in ten random high power fields (40X) according to the percentage of immune positive cells per high power fields as reported in a recent study [33].…”

Section: Immunohistochemical Analysismentioning

confidence: 99%

Antimicrobial and Hepatoprotective Effect of Chitosan Nanoparticles In-vitro and In-vivo Study

El-Shafei

Asaad

Elkhateeb

et al. 2021

JPRI

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Nanotechnology has become an extensive area of study due to the peculiar properties of nanoparticles. Chitosan is considered the most promising material for future applications. The purpose of this study was to highlight the antimicrobial and hepatoprotective properties of Chitosan nanoparticles (CTS), as well as their efficacy against multidrug-resistant pathogens and various applications as a natural antioxidant in the biomedical field. CTS were prepared with or without surfactant (L—lecithin, Tween 80) based on inotropic gelation of chitosan with sodium alginate. The nanoparticle obtained displayed a spherical shape with a particle size ranging from 54.3±20.8 to 1256±16.8 nm, zeta potential ranging from 24±1.2 to 30.8±1.1 mV, and polydispersity index ranging from 0.274±0.09 to 0.553±0.06. Minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) calculations were used to evaluate the antibacterial activity of CTS against four human pathogens: Bacillus subtilis ATCC6633, Staphylococcus aureus NRRLB-767, Escherichia coli ATCC25955, and Pseudomonas aeruginosa ATCC101455. The MIC values were 156.3, 39.4, 78.1, and 78.1 ug/mL, while the MBC values were 500,156.3, 312.5, and 312.5 ug/mL, respectively. S.aureus was the most susceptible, while B. subtilis was the most resistant. The hepatoprotective effect was determined by measuring antioxidant, antiapoptotic, and inflammatory biomarkers, histopathological and immunohistochemical studies. Hepatoprotective results showed a remarkable ameliorative effect against hepatotoxicity induced by CCl4.

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Section: Immunohistochemical Analysismentioning

confidence: 99%

Antimicrobial and Hepatoprotective Effect of Chitosan Nanoparticles In-vitro and In-vivo Study

El-Shafei

Asaad

Elkhateeb

et al. 2021

JPRI

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“…Severe abnormalities affect the intra-renal microcirculation leading to an elevation in intra-renal pressure, activation of the reninangiotensin system, and initiation of intra-renal inflammatory processes ( 2 ). Nephrotoxicity may originate as an adverse reaction against non-steroidal anti-inflammatory drugs, some antibiotics, antineoplastic agents, or xenobiotics ( 3 4 5 ). Therefore, It is of high importance to keep the kidney healthy for all people affected by kidney diseases ( 6 ), besides, it has been very crucial to scout for new nephroprotective agents to improve renal function, renal tissue healing, and regeneration ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Effect of L-carnitine on potassium dichromate-induced nephrotoxicity in rats

Salama

Mostafa

Elgohary

2022

Research in Pharmaceutical Sciences

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Background and purpose: Kidney diseases impose significant global health challenges. Potassium dichromate (PD) is a heavy metal frequently associated with nephrotoxicity. PD prompts oxidative and inflammatory injuries in renal tissues. L-carnitine is a naturally-occurring amino acid commonly used as a supplement. Experimental approach: Forty rats were randomly allocated into 5 groups. Group 1 (normal) received only saline. Nephrotoxicity was induced in the remaining groups by PD (15 mg/kg; i.p). Group 2 served as a nephrotoxic group. Groups 3-5 received L-carnitine (25, 50, and 100 mg/kg; p.o.), respectively for 4 weeks. Findings/Results: PD administration resulted in elevated serum creatinine and blood urea nitrogen accompanied by diminished reduced glutathione and elevated malondialdehyde, tumor necrosis factor-alpha, and transforming growth factor-beta renal tissue contents relative to normal rats. PD also produced apoptotic histopathological injuries and down-regulated PI3K/Akt signaling pathway; signifying ongoing apoptosis. In the current work, L-carnitine use in the selected dose levels resulted in improvement of all the aforementioned serum, renal tissue, and histological parameters relative to nephrotoxic rats. L-carnitine up-regulated PI3K/Akt signaling pathway that was down-regulated post PD use. Conclusion and implications: Collectively, the study highlighted that the possible mechanisms beyond the beneficial effects of L-carnitine are mainly through its antioxidant as well as anti-inflammatory actions. L- carnitine significantly abrogated apoptosis via up-regulation of PI3K/Akt signaling pathway and signified restoration of normal renal cell proliferation and functionality.

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“…Thus, one cannot exclude that drug administration with antioxidant power might help prevent atherosclerotic lesions’ development and progression. Lisinopril, a non-sulfhydryl ACE inhibitor, has been shown to exert scavenger action of free radicals and oxidants in male Wistar rats treated with doxorubicin to induce kidney injury ( Asaad et al, 2021 ). In such experimental conditions, oral lisinopril administration was associated with a striking improvement in antioxidant defense that was impaired by simultaneous doxorubicin administration.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly enough, lisinopril addition to the cellular medium was also associated with anti-apoptotic and anti-fibrotic effects; both phenomena strongly related to the anti-atherosclerotic role ( Hasheminasabgorji and Jha, 2021 ). As far as the anti-fibrotic effect of lisinopril, previous experimental evidence demonstrated that free radical generation is associated with fibrosis due to activation in NADPH oxidase and production of growth factors ( Oktem et al, 2011 ), both phenomena contrasted by lisinopril ( Oktem et al, 2011 ; Saber et al, 2018 ; Asaad et al, 2021 ). Angiotensin II stimulates the NADPH oxidase to produce superoxide and hydrogen peroxide, but lisinopril inhibits the conversion of angiotensin I to angiotensin II, and thus the angiotensin II pro-oxidative effect was downgraded.…”

Section: Discussionmentioning

confidence: 99%

“…Lisinopril is a non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor widely prescribed for treating patients suffering from hypertension and congestive heart failure, both tightly related to coronary heart disease. More recently, lisinopril has been shown to exert an antioxidant effect, lower lipid peroxidation, and anti-inflammatory effect in the kidney of Wistar rats previously treated with doxorubicin ( Asaad et al, 2021 ). Whether lisinopril exerts its antioxidant effects in cardiac cells, which are more exposed to atherosclerosis and coronary heart diseases, is still a matter of debate ( Oktem et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

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Potential Role of Lisinopril in Reducing Atherosclerotic Risk: Evidence of an Antioxidant Effect in Human Cardiomyocytes Cell Line

et al. 2022

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The cellular mechanisms involved in myocardial ischemia/reperfusion injury (I/R) pathogenesis are complex but attributable to reactive oxygen species (ROS) production. ROS produced by coronary endothelial cells, blood cells (e.g., leukocytes and platelets), and cardiac myocytes have the potential to damage vascular cells directly and cardiac myocytes, initiating mechanisms that induce apoptosis, inflammation, necrosis, and fibrosis of myocardial cells. In addition to reducing blood pressure, lisinopril, a new non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor, increases the antioxidant defense in animals and humans. Recently, it has been shown that lisinopril can attenuate renal oxidative injury in the l-NAME-induced hypertensive rat and cause an impressive improvement in the antioxidant defense system of Wistar rats treated with doxorubicin. The potential effect of lisinopril on oxidative damage and fibrosis in human cardiomyocytes has not been previously investigated. Thus, the present study aims to investigate the effect of different doses of lisinopril on oxidative stress and fibrotic mediators in AC16 human cardiomyocytes, along with a 7-day presence in the culture medium. The results revealed that AC16 human cardiomyocytes exposed to lisinopril treatment significantly showed an upregulation of proteins involved in protecting against oxidative stress, such as catalase, SOD2, and thioredoxin, and a reduction of osteopontin and Galectin-3, critical proteins involved in cardiac fibrosis. Moreover, lisinopril treatment induced an increment in Sirtuin 1 and Sirtuin 6 protein expression. These findings demonstrated that, in AC16 human cardiomyocytes, lisinopril could protect against oxidative stress and fibrosis via the activation of Sirtuin 1 and Sirtuin 6 pathways.

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Anti-oxidant impact of Lisinopril and Enalapril against acute kidney injury induced by doxorubicin in male Wistar rats: involvement of kidney injury molecule-1

Cited by 26 publications

References 34 publications

Antimicrobial and Hepatoprotective Effect of Chitosan Nanoparticles In-vitro and In-vivo Study

Antimicrobial and Hepatoprotective Effect of Chitosan Nanoparticles In-vitro and In-vivo Study

Effect of L-carnitine on potassium dichromate-induced nephrotoxicity in rats

Potential Role of Lisinopril in Reducing Atherosclerotic Risk: Evidence of an Antioxidant Effect in Human Cardiomyocytes Cell Line

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