Effect of pre- and posttreatment of losartan in feline model of
myocardial ischemic-reperfusion injury

Kumari, Rajesh; Manchanda, S. C.; Maulik, Subir Kumar

doi:10.1358/mf.2004.26.1.793471

Cited by 5 publications

(3 citation statements)

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“…In addition, losartan could repress liver injury caused by ischemia/reperfusion via the regulation of PPARγg activation, which was widely established as a protective regulator of ischemia/reperfusion injury [26]. Moreover, losartan was also revealed as a repressor of myocardial ischemic/reperfusion injury [27], vascular injury induced by advanced glycosylation [28], brain injury [29], and endothelial damage associated with hypertension and type 2 diabetes mellitus [30]. Our finding of the inhibitory effects of losartan on the AKI rat model provided further evidence of the wide range of tissues regulated by losartan.…”

Section: Discussionmentioning

confidence: 99%

Rat mRNA expression profiles associated with inhibition of ischemic acute kidney injury by losartan

Peng

et al. 2019

Bioscience Reports

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Objective: Losartan was reported to inhibit the progression of acute kidney injury (AKI), but little is known about the underlying pharmacological mechanisms. In the present study, the mRNA expression profiles in ischemic AKI rat kidney altered by losartan treatment were analyzed by next-generation deep sequencing technology. Methods: Ischemia and reperfusion treatment was applied to induce AKI in Sprague–Dawley (SD) rats. The urea and creatinine contents in rat blood were measured. H&E staining was performed to evaluate the histological alteration of rat kidney tissues under a microscope. The TUNEL method was applied to analyze apoptosis in rat kidney tissues. The mRNA profiles in rat kidney were analyzed using next-generation deep sequencing. Differential gene expression was confirmed by quantitative qRT-PCR. Results: The rat model of AKI induced by ischemia and reperfusion showed significant increases in urea and creatinine levels, accompanied by a disrupted kidney tubular structure and renal cell apoptosis. Losartan treatment effectively inhibited the changes in urea and creatinine, tubular structure, and apoptosis in AKI rat kidney. A large number of mRNAs were found to be differentially expressed in the kidneys of AKI rats treated with losartan, which are involved in multiple processes and signaling pathways. The expression of nine differentially expressed genes such as monocyte chemoattractant protein-1 (CCL2) and suppressor of cytokine signaling 3 (SOCS3) was confirmed by qRT-PCR and Western blot. Conclusion: Losartan caused significant alterations in the gene expression profile in AKI rat kidney, which mediated its anti-AKI effects.

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Section: Discussionmentioning

confidence: 99%

Rat mRNA expression profiles associated with inhibition of ischemic acute kidney injury by losartan

Peng

et al. 2019

Bioscience Reports

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“…Originally, losartan, an ANG II type-1 (AT 1 )-receptor antagonist was used for the treatment of hypertension, and has been recently studied for its varied effects in different animal models (Hashimoto et al 1999, Suzuki et al 2001, Kumari et al 2004, Silva et al, 2009.…”

Section: Introductionmentioning

confidence: 99%

AT1-receptor mediated vascular damage in myocardium, kidneys and liver in rats

Vailati

Rocha

Matsubara³

et al. 2010

Pesq. Vet. Bras.

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The systemic aspect of vascular damage induced by angiotensin II (ANG II) has been poorly explored in the literature. Considering the presence of ANG II and its specific receptor AT1, in several organs, all tissues might be potentially affected by its effects. The aims of this study were: To evaluate the early histological changes in the heart, liver and kidneys, produced by ANG II infusion, to evaluate the protective effect of losartan. Wistar rats were distributed into three groups: control (no treatment), treated with ANG II, and treated with ANG II + losartan. ANG II was continuously infused over 72 hours by subcutaneous osmotic pumps. Histological sections of the myocardium, kidneys and liver were stained and observed for the presence of necrosis. There were ANG II-induced perivascular inflammation and necrosis of the arteriolar wall in the myocardium, kidney, and liver by, which were partially prevented by losartan. There was no significant correlation between heart and kidney damage. Tissue lesion severity was lower than that of vascular lesions, without statistical difference between groups. ANG II causes vascular injury in the heart, kidneys and liver, indicating a systemic vasculotoxic effect; the mechanisms of damage/protection vary depending on the target organ; perivascular lesions may occur even when anti-hypertensive doses of losartan are used.

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“…Η εκτίμηση του οξειδωτικού φορτίου έγινε με την μέτρηση των TBARS στο φλεβικό αίμα του στεφανιαίου κόλπου. Η ποσότητα των TBARS που ανιχνεύεται στους βιολογικούς ιστούς ή στο αίμα αποτελεί ένα έμμεσο δείκτη οξειδωτικού φορτίου που χρησιμοποιείται ευρέως σε πειραματικές και κλινικές μελέτες383,430,431 . Η μέτρηση της συγκέντρωσης των TBARS στο αίμα του στεφανιαίου κόλπου έγινε σε διαφορετικές χρονικές στιγμές κατά την διάρκεια του πειράματος έτσι ώστε να προσδιοριστεί πέραν της απολύτου τιμής συγκέντρωσης τους και η κινητική τους μετά την επαναιμάτωση.…”

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Επίδραση Αντιοξειδωτικών Στη Μυοκαρδιακή Βλάβη Που Προκαλείται Μετά Ισχαιμία - Επαναιμάτωση

Nikas¹,

Νίκας²

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Effect of pre- and posttreatment of losartan in feline model of myocardial ischemic-reperfusion injury

Cited by 5 publications

References 0 publications

Rat mRNA expression profiles associated with inhibition of ischemic acute kidney injury by losartan

Rat mRNA expression profiles associated with inhibition of ischemic acute kidney injury by losartan

AT1-receptor mediated vascular damage in myocardium, kidneys and liver in rats

Επίδραση Αντιοξειδωτικών Στη Μυοκαρδιακή Βλάβη Που Προκαλείται Μετά Ισχαιμία - Επαναιμάτωση

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