The Effect of Carvacrol on IL-1β and Nitric Oxide Levels on Lipopolysaccharide-induced Acute Renal Injury in Male Rats
محورهای موضوعی :
Alireza Mortazavi
1
,
Mahmoud Hosseini
2
,
Farimah Beheshti
3
,
Zahra Hakimi
4
,
Gholam Hassan Vaezi
5
,
Hossain Mohammad Pour Kargar
6
1 - Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
2 - Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran |Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mash had, Iran
3 - Neuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran |Department of Physiology, Faculty of Paramedical Sciences, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
4 - Department of Physiology, School of Medicine, Ghalib University, Herat, Afghanistan |Faculty of Medicine, Ghalib University, Herat, Afghanistan
5 - Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
6 - Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran |Faculty of Pharmacy, Islamic Azad University, Damghan Branch, Damghan, Iran
تاریخ دریافت : 1400/04/01
تاریخ پذیرش : 1402/02/17
تاریخ انتشار : 1402/12/11
کلید واژه:
Inflammation,
Carvacrol,
kidney,
Lipopolysaccharide,
چکیده مقاله :
Carvacrol is a phenolic monoterpenoid compound that has antibacterial, antifungal, anti-cancer, and anti-inflammatory effects. Lipopolysaccharide (LPS) is derived from the outer cell wall of gram-negative bacteria and is responsible for acute kidney injury. In this research, the protective effect of carvacrol on lipopolysaccharide-induced acute kidney injury was studied. For this purpose, 40 male Wistar rats (200-250 g) were used. Animals were randomly divided into 5 equal groups: 1) control, 2) LPS group, 3) LPS+carvacrol (25 mg kg-1), 4) LPS+carvacrol (50 mg kg-1) and 5) LPS+carvacrol (100 mg kg-1). To induce acute renal injury, daily 1 mg kg-1 LPS for 2 weeks was injected intraperitoneally. Carvacrol was administered intraperitoneally daily for 30 minutes before LPS injection. LPS-induced kidney injury was evaluated by blood urea nitrogen (BUN), serum creatinine, and nitric oxide levels in kidney tissue by spectrophotometric methods. The level of the interleukin 1 beta was detected by ELISA in the kidney. Our results showed that LPS injection increased BUN, creatinine, nitric oxide, and IL-1β levels (P <0.001). Pretreatment with carvacrol reduced BUN at 25 mg kg-1 (P <0.001), 50 mg kg-1 (P <0.01), and 100 mg kg-1 (P <0.001) doses, nitric oxide at 25 mg kg-1 (P <0.05), 50 mg kg-1(P <0.01) and 100 mg kg-1(P <0.001) doses, and IL-1β levels (P <0.001) at all doses significantly but did not affect serum creatinine. These results indicate that carvacrol has an anti-inflammatory effect and protects kidneys against LPS by reducing pro-inflammatory mediators such as IL-1β and nitric oxide.
چکیده انگلیسی:
Carvacrol is a phenolic monoterpenoid compound that has antibacterial, antifungal, anti-cancer, and anti-inflammatory effects. Lipopolysaccharide (LPS) is derived from the outer cell wall of gram-negative bacteria and is responsible for acute kidney injury. In this research, the protective effect of carvacrol on lipopolysaccharide-induced acute kidney injury was studied. For this purpose, 40 male Wistar rats (200-250 g) were used. Animals were randomly divided into 5 equal groups: 1) control, 2) LPS group, 3) LPS+carvacrol (25 mg kg-1), 4) LPS+carvacrol (50 mg kg-1) and 5) LPS+carvacrol (100 mg kg-1). To induce acute renal injury, daily 1 mg kg-1 LPS for 2 weeks was injected intraperitoneally. Carvacrol was administered intraperitoneally daily for 30 minutes before LPS injection. LPS-induced kidney injury was evaluated by blood urea nitrogen (BUN), serum creatinine, and nitric oxide levels in kidney tissue by spectrophotometric methods. The level of the interleukin 1 beta was detected by ELISA in the kidney. Our results showed that LPS injection increased BUN, creatinine, nitric oxide, and IL-1β levels (P <0.001). Pretreatment with carvacrol reduced BUN at 25 mg kg-1 (P <0.001), 50 mg kg-1 (P <0.01), and 100 mg kg-1 (P <0.001) doses, nitric oxide at 25 mg kg-1 (P <0.05), 50 mg kg-1(P <0.01) and 100 mg kg-1(P <0.001) doses, and IL-1β levels (P <0.001) at all doses significantly but did not affect serum creatinine. These results indicate that carvacrol has an anti-inflammatory effect and protects kidneys against LPS by reducing pro-inflammatory mediators such as IL-1β and nitric oxide.
منابع و مأخذ:
Goodman C.W., Brett A.S., 2017. Gabapentin and pregabalin for pain—is increased prescribing a cause for concern? New England Journal of Medicine. 377(5), 411-414.
Shum H.P., Yan W.W., Chan T.M., 2016. Recent knowledge on the pathophysiology of septic acute kidney injury: a narrative review. Journal of Critical Care. 31(1), 82-89.
Cohen J., 2002. The immunopathogenesis of sepsis. Nature. 420(6917), 885-891.
Hewett J.A., Roth R.A., 1993. Hepatic and extrahepatic pathobiology of bacterial lipopolysaccharides. Pharmacological Reviews. 45 (4), 381-411.
Yuan H., Perry C.N., Huang C., Iwai-Kanai E., Carreira R.S., Glembotski C.C., Gottlieb R.A., 2009. LPS-induced autophagy is mediated by oxidative signaling in cardiomyocytes and is associated with cytoprotection. American Journal of Physiology-Heart and Circulatory Physiology. 296(2), 470-479.
Aragno M., Cutrin J.C., Mastrocola R., Perrelli M.G., Restivo F., Poli G., Danni O., Boccuzzi G., 2003. Oxidative stress and kidney dysfunction due to ischemia/reperfusion in rat: attenuation by dehydroepiandrosterone. Kidney International. 64(3), 836-843.
Bogdan C., 2001. Nitric oxide and the immune response. Nature Immunology. 2(10), 907-916.
Jansen A., Cook T., Taylor G. M., Largen P., Riveros-Moreno V., Moncada S., Cattell V., 1994. Induction of nitric oxide synthase in rat immune complex glomerulonephritis. Kidney International. 45(4), 1215-1219.
Baylis C., Mitruka B., Deng A., 1992. Chronic blockade of nitric oxide synthesis in the rat produces systemic hypertension and glomerular damage. The Journal of Clinical Investigation. 90(1), 278-281.
Zhang C., Walker L.M., Mayeux P.R., 2000. Role of nitric oxide in lipopolysaccharide-induced oxidant stress in the rat kidney. Biochemical Pharmacology. 59(2), 203-209.
Faas M., Schuiling G., Valkhof N., Baller J., Bakker W., 1998. Superoxide–Mediated Glomerulopathy in the Endotoxin–Treated Pregnant Rat. Kidney and Blood Pressure Research. 21(6), 432-437.
White S.B., 2011. Antibacterial efficacy of phosvitin, carvacrol, or nisin alone or combined against foodborne human enteric pathogens. Graduate Theses and Dissertations. 10(151), 114-117
Suntres Z.E., Coccimiglio J., Alipour M., 2015. The bioactivity and toxicological actions of carvacrol. Critical Reviews in Food Science and Nutrition. 55(3), 304-318.
Lima Mda S., Quintans-Júnior L.J., de Santana W.A., Martins Kaneto C., Pereira Soares M.B., Villarreal C.F., 2013. Anti-inflammatory effects of carvacrol: evidence for a key role of interleukin-10. Eur J Pharmacol. 699 (1-3), 112-117.
Mortazavi A., Mohammad Pour Kargar H., Beheshti F., Anaeigoudari A., Vaezi G., Hosseini M., 2021. The effects of carvacrol on oxidative stress, inflammation, and liver function indicators in a systemic inflammation model induced by lipopolysaccharide in rats. Int J Vitam Nutr Res. 1-11.
Landa P., Kokoska L., Pribylova M., Vanek T., Marsik P., 2009. In vitro anti-inflammatory activity of carvacrol: Inhibitory effect on COX-2 catalyzed prostaglandin E 2 biosynthesisb. Archives of Pharmacal Research. 32(1), 75-78.
Uyanoglu M., Canbek M., Ceyhan E., Senturk H., Bayramoglu G., Gunduz O., Ozen A., Turgak O., 2011. Preventing organ injury with carvacrol after renal ischemia/reperfusion. Journal of Medicinal Plants Research. 5(1), 72-80.
Ozer E.K., Goktas M.T., Toker A., Bariskaner H., Ugurluoglu C., Iskit A.B., 2017. Effects of carvacrol on survival, mesenteric blood flow, aortic function and multiple organ injury in a murine model of polymicrobial sepsis. Inflammation. 40(5), 1654-1663.
Hotta M., Nakata R., Katsukawa M., Hori K., Takahashi S., Inoue H., 2010. Carvacrol, a component of thyme oil, activates PPARalpha and gamma and suppresses COX-2 expression. J Lipid Res. 51(1), 132-139.
Mir S.M., Ravuri H.G., Pradhan R.K., Narra S., Kumar J.M., Kuncha M., Kanjilal S., Sistla R., 2018. Ferulic acid protects lipopolysaccharide-induced acute kidney injury by suppressing inflammatory events and upregulating antioxidant defenses in Balb/c mice. Biomed Pharmacother. 100, 304-315.
Hosseini M., Beheshti F., Anaeigoudari A., 2020. Improving Effect of Aminoguanidine on Lipopolysaccharide-Caused Kidney Dysfunction in Rats. Saudi Journal of Kidney Diseases and Transplantation. 31(5), 1025-1033.
Zaheri M., Ebrahimi Vosta Kalai S., Cheraghi J., 2011. Protective effect of aerial parts extract of Scrophularia striata on cadmium and mercury-induced nephrotoxicity in rat. Journal of Babol University of Medical Sciences. 13(4), 48-53.
Granger D.L., Taintor R.R., Boockvar K.S., Hibbs Jr J.B., 1996. Measurement of nitrate and nitrite in biological samples using nitrate reductase and Griess reaction. Methods in Enzymology. 268, 142-151.
Liu H.H., Zhao T.B., Li Z.L., 2008. Changes of serum urea and creatinine concentrations in rats with lipopolysaccharide and heat co-exposure. Nan fang yi ke da xue xue bao. Journal of Southern Medical University. 28(1), 86-88.
Schor N., 2002. Acute renal failure and the sepsis syndrome. Kidney International. 61(2), 764-776.
Liu M., Bing G., 2011. Lipopolysaccharide animal models for Parkinson's disease. Parkinsons Dis. 327089.
Bussolati B., David S., Cambi V., Tobias P.S., Camussi G., 2002. Urinary soluble CD14 mediates human proximal tubular epithelial cell injury induced by LPS. Int J Mol Med. 10(4), 441-449.
Fu H., Hu Z., Di X., Zhang Q., Zhou R., Du H., 2016. Tenuigenin exhibits protective effects against LPS-induced acute kidney injury via inhibiting TLR4/NF-κB signaling pathway. European Journal of Pharmacology. 791, 229-234.
Faggioni R., Fantuzzi G., Fuller J., Dinarello C.A., Feingold K.R., Grunfeld C., 1998. IL-1β mediates leptin induction during inflammation. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 274(1), R204-R208.
Xu C., Chang A., Hack B.K., Eadon M.T., Alper S.L., Cunningham P.N., 2014. TNF-mediated damage to glomerular endothelium is an important determinant of acute kidney injury in sepsis. Kidney International. 85(1), 72-81.
Kelm M., 1999. Nitric oxide metabolism and breakdown. Biochim Biophys Acta. 1411 (2-3), 273-289.
Sadegh M., Sakhaie M.H., 2018. Carvacrol mitigates proconvulsive effects of lipopolysaccharide, possibly through the hippocampal cyclooxygenase-2 inhibition. Metab Brain Dis. 33(6), 2045-2050.
Delanaye P., Cavalier E., Pottel H., 2017. Serum creatinine: not so simple! Nephron. 136(4), 302-308.
Papadakis M.A., Arieff A.I., 1987. Unpredictability of clinical evaluation of renal function in cirrhosis: prospective study. The American Journal of Medicine. 82(5), 945-952.
Liu Q., Zhao H., Gao Y., Meng Y., Zhao X.X., Pan S.N., 2018. Effects of dandelion extract on the proliferation of rat skeletal muscle cells and the inhibition of a lipopolysaccharide-induced inflammatory reaction. Chinese Medical Journal. 131(14), 1724.
Ozkok E., Yorulmaz H., Ates G., Aksu A., Balkis N., Şahİn Ö., Tamer S., 2016. Amelioration of energy metabolism by melatonin in skeletal muscle of rats with LPS induced endotoxemia. Physiological Research. 65(5), 833-842
Gardiner S.M., Kemp P.A., March J.E., Bennett T., 1999. Influence of FR 167653, an inhibitor of TNF-alpha and IL-1, on the cardiovascular responses to chronic infusion of lipopolysaccharide in conscious rats. J Cardiovasc Pharmacol. 34(1), 64-69.