Experimental models of kidney diseases to study pathogenetic mechanisms and efficacy of pharmacological correction against the background of comorbid pathology

Authors

  • N. M. Seredynska State Institution “Institute of Pharmacology and Toxicology of the National Academy of Medical Sciences of Ukraine”, Kyiv,
  • N. D. Filipets Higher State Educational Establishment of Ukraine “Bukovinian State Medical University”, Chernivtsi,
  • O. O. Filipets Higher State Educational Establishment of Ukraine “Bukovinian State Medical University”, Chernivtsi,
  • K. V. Slobodian Higher State Educational Establishment of Ukraine “Bukovinian State Medical University”, Chernivtsi,
  • A. I. Hozhenko State Enterprise “Ukrainian Research Institute of Transport Medicine of the Ministry of Public Health of Ukraine”, Odesa,

DOI:

https://doi.org/10.14739/2310-1210.2019.3.169197

Keywords:

experimental animal models, kidney, comorbidity

Abstract

 

The aim of our study is to report about modern models of kidney diseases associated with other pathological conditions for experimental studies of pathogenic mechanisms and efficacy of pharmacological correction.

The study deals with experimental models reasonably to be applied in investigation of comorbid pathology pathogenesis and efficacy of its pharmacological correction. The attention is focused on the models of cardio-renal, hepatic-renal syndromes and multiple organ hypoxic histochemical injury simulated in laboratory rats. These models are characterized by easy modeling, simulation of comorbidity pathogenesis, acute and chronic periods of diseases available, induced by the antibiotic Doxorubicin or exotoxins – corrosive sublimate, sodium nitrite, and 2,4-dinitrophenol.

Conclusions. The models of cardio-renal, hepatic-renal syndromes and hypoxic histochemical injury of the body are found to be optimal to perform multipurpose studies of physiological, pathophysiological, pharmacological directions with maximal similarity of the results obtained to clinical-therapeutic peculiarities of comorbid pathology.

References

Gozhenko, A.I. (2018). Teoriya bolezni [Theory of disease]. Odesa: Fenix. [in Russian].

Gozhenko, A. I. (2016). Funkcional'no-metabolicheskij kontinuum [Functional-metabolic continuum]. Zhurnal natsionalnoi akademii medychnykh nauk Ukrayiny, 22(1), 3–8. [in Russian].

Seredinska, N. M., Yadlovskyi, O. E., Bershova, T. A., Omelyanenko, Z. P., Khomenko, V. S., & Kirichok, L. M. (2015). Otsinka intehralnykh pokaznykiv zhyttiediialnosti v shchuriv za umov kombinovanoho zastosuvannia nesteroidnykh protyzapalnykh zasobiv ta antahonista kaltsiiu na modeli revmatoidnoho artrytu, poiednanoho z arterialnoiu hipertenziieiu [The evaluation of rat`s integral indices after combined use of NSAIDs and calcium antagonist at the rheumatoid arthritis model in conjunction with arterial hypertension]. Farmakolohiia ta likarska toksykolohiia, 4–5, 69–78. [in Ukrainian].

Seredinskaya, N. N., Sushinskaya, A. A., Chomenko, V. S., Omelyanenko, Z. P., & Bershova, T. A. (2016). Kardiotropna diia tselekoksybu za kombinovanoho zastosuvannia z amlodypinom u shchuriv na tli adiuvantnoho artrytu, poiednanoho z arterialnoiu hipertenziieiu [Cardiotropic action of combined use of celecoxib and amlodipine in rats sicked on adjuvant arthritis coupled with arterial hypertension]. Farmatsevtychnyi zhurnal, 1, 91–97. [in Ukrainian].

Cho, S., & Yang, J. (2018). What Do Experimental Models Teach Us About Comorbidities in Stroke? Stroke, 49(2), 501–507. doi: 10.1161/STROKEAHA.117.017793

Freeman, W. D., & Wadei, H. M. (2015). A brain-kidney connection: the delicate interplay of brain and kidney physiology. Neurocrit Care, 22(2), 173–175. doi: 10.1007/s12028-015-0119-8

Nakagawa, N., & Hasebe, N. (2016). Pathophysiology of cerebro-cardio-renal continuum in patients with left ventricular hypertrophy. J Card Fail, 22(9), 157. doi: https://doi.org/10.1016/j.cardfail.2016.07.035

Husain-Syed, F., McCullough, P. A., Birk, H. W., Renker, M., Brocca, A., Seeger, W., et al. (2015). Cardio-Pulmonary-Renal Interactions: A Multidisciplinary Approach. J Am Coll Cardiol, 65(22), 2433–2448. doi: 10.1016/j.jacc.2015.04.024

Mindikoglu, A. L., & Pappas, S. C. (2018). New Developments in Hepatorenal Syndrome. Clin Gastroenterol Hepatol, 16(2), 162–177. doi: 10.1016/j.cgh.2017.05.041

Shchekochikhin, D., Schrier, R. W., & Lindenfeld, J. (2013). Cardiorenal syndrome: pathophysiology and treatment. Curr Cardiol Rep, 15(7), 380. doi: 10.1007/s11886-013-0380-4

De Vecchis, R., Baldi, C., & Di Biase, G. (2016). Poor concordance between different definitions of worsening renal function in patients with acute exacerbation of chronic heart failure: a retrospective study. Minerva Cardioangiol, 64(2), 127–137.

Di Lullo, L., Bellasi, А., & De Pascalis, А. (2017). Hypertension, type IV cardiorenal syndrome and chronic kidney disease: Pathophysiological and therapeutical approach. World J Hypertens, 7(1), 10–18. doi: 10.5494/wjh.v7.i1.10

Szymanski, M. K., de Boer, R. A., Navis, G. J., van Gilst, W. H., & Hillege, H. L. (2012). Animal models of cardiorenal syndrome: a review. Heart Failure Reviews, 17(3), 411–420. doi: 10.1007/s10741-011-9279-6

Ichikawa, Y., Ghanefar, M., Bayeva, M., Wu, R., Khechaduri, A., Naga Prasad, S. V., et al. (2014). Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. J Clin Invest, 124(2), 617–630. doi: 10.1172/JCI72931

Cardinale, D., Colombo, A., Bacchiani, G., Tedeschi, I., Meroni, C. A.,Veglia, F., et al. (2015). Early detection of anthracycline cardiotoxicity and improvement with heart failure therapy. Circulation, 131(22), 1981–1988. doi: 10.1161/CIRCULATIONAHA.114.013777

Polegato, B. F., Minicucci, M. F., Azevedo, P. S., Carvalho, R. F., Chiuso-Minicucci, F., Pereira, E. J., et al. (2015). Acute doxorubicin-induced cardiotoxicity is associated with matrix metalloproteinase-2 alterations in rats. Cell Physiol Biochem, 35(5), 1924–33. doi: 10.1159/000374001

Моkhort, M. А, Seredinska, N. M., & Кiricheк, L. М. (2010). Kardiotoksychni efekty doksorubitsynu i dotsilnist yikh farmakolohichnoi korektsii antahonistamy kaltsiiu dyhidropirydynovoho riadu ta aktyvatoramy ATF-zalezhnykh kaliievykh kanaliv huanidynovoho riadu [Cardiotoxic effects of doxorubicin and expediency of its pharmacological correction by dihydropyridinic line calcium antagonists and by guanidine line ATF-sensitive potassium canals activators]. Farmakolohiia ta likarska toksykolohiia, 4(17), 35–44. [in Ukrainian].

Saenko, Yu. V., Shutоv, А. M., & Мusinа, Р. Kh. (2006). K mekhanizmu toksicheskogo dejstviya doksorubicina na pochki [On the меchanism of toxic effect of doxorubicin on the kidneys]. Nefrologiya, 10(4), 72–76 [in Russian].

Radwan, R. R., Shaban, E. A., Kenawy, S. A., & Salem, H. A. (2012). Protection by low-dose γ radiation on doxorubicin-induced nephropathy in rats pretreated with curcumin, green tea, garlic or L-carnitine. Bulletin of Faculty of Pharmacy, Cairo University, 50(2), 133–140. doi: 10.1016/j.bfopcu.2012.09.002

Nagai, K., Fukuno, S., Otani, K., Nagamine, Y., Omotani, S., Hatsuda, Y., et al. (2018). Prevention of doxorubicin-induced renal toxicity by theanine in rats. Pharmacology, 101(3–4), 219–224. doi: 10.1159/000486625

Hrenák, J., Arendášová, K., Rajkovičová, R., Aziriová, S., Repová, K., Krajčírovičová, K., et al. (2013). Protective effect of captopril, olmesartan, melatonin and compound 21 on doxorubicin-induced nephrotoxicity in rats. Physiol Res, 62(l), 181–189.

Kalender, Y., Yel, M., & Kalender, S. (2005). Doxorubicin hepatotoxicity and hepatic free radical metabolism in rats. The effects of vitamin E and catechin. Toxicology, 209(1), 39–45. doi: 10.1016/j.tox.2004.12.003

El-Moselhy, M. A., & El-Sheikh, A. A. K. (2014). Protective mechanisms of atorvastatin against doxorubicin-induced hepato-renal toxicity. Biomed Pharmacother, 68(1), 101–110. doi: 10.1016/j.biopha.2013.09.001

Zupanets, I. A., Vetrova, К. V., Sakharova, T. S., & Derkach, R. V. (2014). Korektsiia doksorubitsynindukovanoi hepatotoksychnosti pokhidnymy hliukozaminu ta yikh kombinatsiiamy z kvertsetynom v eksperymenti na shchurakh [Correction of doxorubicin-induced hepatotoxicity by glucosamine derivatives and their combinations with quercetin in rats]. Klinichna farmatsiia, 2, 4–9. [in Ukrainian].

Wang, Y., Mei, X., Yuan, J., Lu, W., Li, B., & Xu, D. (2015). Taurine zinc solid dispersions attenuate doxorubicin-induced hepatotoxicity and cardiotoxicity in rats. Toxicol Appl Pharmacol, 289(1), 1–11. doi: 10.1016/j.taap.2015.08.017

Gozhenko, А. I, & Sluchenko, А. N. (2006). Funkcional'noe sostoyanie pochek v usloviyakh vodnoj i solevoj nagruzok pri beremennosti u krys na fone sulemovoj nefropatii [Functional state of the kidneys under conditions of water and salt loads in pregnant rats against the background of sublimate nephropathy]. Nephrologiya, 10(1), 72–76. [in Russian].

Agha, F. E., Youness, E. R., Selim, M. M. H., & Ahmed, H. H. (2014). Nephroprotective potential of selenium and taurine against mercuric chloride induced nephropathy in rats. Renal Failure, 36(5), 704–716. doi: 10.3109/0886022X.2014.890012

Gozhenko, A. I, & Filipets, N. D. (2013). Nefrotropnye e'ffekty pri aktivacii adenozintrifosfatchuvstvitel'nykh kalievykh kanalov v zavisimosti ot funktsional'nogo sostoyaniya pochek krys [Тhe renotropic effects of adenosine triphosphate-sensitive potassium channel activation depending on the functional state of kidneys in rats]. Nephrologiya, 17(2), 87–90. [in Russian].

Filipets, N. D, & Gozhenko, A. I. (2014). Sravnitel'naya ocenka nefroprotektivnykh svojstv modulyatorov kalievykh i kal'ciyevykh kanalov pri e'ksperimental'nom porazhenii pochek [Comparative assessment of nephroprotective properties of potassium and calcium channel modulators in experimental renal injury]. E'ksperimental'naya i klinicheskaya farmakologiya, 77(1), 10–12. [in Russian].

Oda, S. S., & El-Ashmawy, I. M. (2012). Protective effect of silymarin on mercury-induced acute nephro-hepatotoxicity in rats. Veterinaria, 9(4), 376–383. doi: 10.5829/idosi.gv.2012.9.4.6510

Liu, W., Xu, Z., Li, H., Guo, M., Yang, T., Feng, S., et al. (2017). Protective effects of curcumin against mercury-induced hepatic injuries in rats, involvement of oxidative stress antagonism, and Nrf2-ARE pathway activation. Hum Exp Toxicol, 36(9), 949–966. doi: 10.1177/0960327116677355

Rohovyi, Yu. Ye., Zlotar, O.V., & Filipova, L.O. (2012). Patofiziolohiia hepatorenalnoho syndromu na poliurychnii stadii sulemovoi nefropatii. [Pathophysiology of hepatorenal syndrome at the polyuric stage of sublimate nephropathy]. Chernivtsi: Medychnyi universytet. [in Ukrainian].

Hirakawa, Y., Tanaka, T., & Nangaku, M. (2017). Renal Hypoxia in CKD; Pathophysiology and Detecting Methods. Front Physiol, (8), 99. doi: 10.3389/fphys.2017.00099

Handzlik, M. K., Constantin-Teodosiu, D., Greenhaff, P. L., & Cole, M. A. (2018). Increasing cardiac pyruvate dehydrogenase flux during chronic hypoxia improves acute hypoxic tolerance. J Physiol, 596(15), 3357–3369. doi: 10.1113/JP275357

Schiffer, T. A., & Friederich-Persson, M. (2017). Mitochondrial Reactive Oxygen Species and Kidney Hypoxia in the Development of Diabetic Nephropathy. Front Physiol, 8, 211. doi: 10.3389/fphys.2017.00211

Gozhenko, A. I, & Filipets, N. D. (2014). Funktsionalnyi stan nyrok pislia aktyvatsii adenozyntryfosfatchutlyvykh kaliievykh kanaliv pry eksperymentalnii hostrii hipoksii [Тhe functional state of kidneys after adenosine triphosphate sensitive potassium channels activation in experimental acute hypoxia] Fiziolohichnyi zhurnal, 60(4), 22–9 [in Ukrainian].

Putilina, F. E., & Еshchenko, N. D. (1971). Vliyaniye gipoksii i 2,4-dinitrofenola na laktatdegidrogenaznuyu reakciyu v mozgu [Effect of hypoxia and 2,4-dinitrophenol on lactate dehydrogenase activity in brain, liver and kidneys]. Voprosy medicinskoj khimii, 17(2), 161–165. [in Russian].

Al-Rasheed, N. M., Fadda, L. M., Attia, H. A., Ali, H. M., & Al-Rasheed, N. M. (2017). Quercetin inhibits sodium nitrite-induced inflammation and apoptosis in different rats organs by suppressing Bax, HIF1-α, TGF-β, Smad-2, and AKT pathways. J Biochem Mol Toxicol, 31(5). doi: 10.1002/jbt.21883

Friederich-Persson, M., Thörn, E., Hansell, P., Nangaku, M., Levin, M., & Palm, F. (2013). Кidney hypoxia, due to increased oxygen consumption, induces nephropathy independently of hyperglycemia and oxidative stress. Hypertension, 62(5), 914–919. doi: 10.1161/HYPERTENSIONAHA.113.01425

Boihuk, Т. М., Rohovyi, Yu. Ye, & Popovych, H. B. (2012). Patofiziolohiia hepato-renalnoho syndromu pry hemichnii hipoksii [Pathophysiology of the hepatic-renal syndrome at the hemic hypoxia]. Chernivtsi: Medychnyi universytet. [in Ukrainian].

Filipets, N. D., Sirman, V. M., & Gozhenko, A.І . (2014). Vliyaniye modulyatorov ionnykh kanalov na funkciyu pochek v nachal'noj stadii razvitiya gistogemicheskoj gipoksii [Effects of modulators of ion channels on renal function at the initial stage of development of histohemic hypoxia]. Zhurnal natsionalnoi akademii medychnykh nauk Ukrainy, 20(4), 483–487. [in Russian].

Gozhenko A. I., Filipets N. D., & Zukow W. (2013). Flokaline and diltiazem renoprotector properties in chronization hypoxic nephropathy. Journal of Health Sciences, 3(12), 389–398.

Downloads

How to Cite

1.
Seredynska NM, Filipets ND, Filipets OO, Slobodian KV, Hozhenko AI. Experimental models of kidney diseases to study pathogenetic mechanisms and efficacy of pharmacological correction against the background of comorbid pathology. Zaporozhye Medical Journal [Internet]. 2019May31 [cited 2024Dec.24];(3). Available from: http://zmj.zsmu.edu.ua/article/view/169197

Issue

No. 3 (2019)

Section

Review

License

Authors who publish with this journal agree to the following terms:

    1. Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.  Лицензия Creative Commons
    2. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
    3. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access)