The role of proinflammatory cytokines on liver damage after pentylenetetrazole-induced acute and chronic epilepsy models in rats

Yıl 2021, Cilt: 43 Sayı: 2, 195 - 200, 01.07.2021

Engin Altinkaya Hilmi Ataseven

https://doi.org/10.7197/cmj.931067

Öz

Abstract
Objectives: The mechanisms of acute liver failure resulting from epilepsy are poorly defined and appear to be multifactorial, including hypoxia and steatosis. The role of inflammation on liver damage after seizures is unclear. This study aimed to investigate the relationship between proinflammatory cytokines and liver damage after pentylenetetrazole-induced acute and chronic epilepsy models in rats.
Materials and methods: Male Wistar albino adult rats (n = 18), weighing 220–240 g, were used in the experiment. The animals were divided into three groups: (1) Control Group (Control; n = 6); rats were treated with a single dose of saline intraperitoneally (i.p.), (2) Acute Epileptic Model Group (n = 6); rats were treated with a single dose of i.p. PTZ (45 mg/kg), (3) Chronic Epileptic Model Group (n = 6); rats were treated with repeated doses of i.p. PTZ (35 mg/kg) every other day for 15(fifteen) times.
Result: There was a significant difference between the control and acute epileptic model in terms of serum AST, TNF-α, IL-1 β and IL-6 parameters (p<0.05). On the other hand, there was a significant difference between the acute and chronic epileptic models in the serum AST, TNF-α and IL-6 parameters (p<0.05).
Conclusions: As a result, while liver damage is secondary to hypoxia during epileptic seizures, multifactorial causes are blamed. Proinflammatory cytokines that increase in the liver after these factors may be responsible for liver damage in acute epileptic seizures. Compensation mechanisms such as antioxidant defence mechanism in chronic epileptic seizures may prevent liver damage.

Anahtar Kelimeler

Epilepsy, liver injury, pentylenetetrazol, proinflammatory cytocine

Kaynakça

• [1] B. L. Kroner, M. Fahimi, W. D. Gaillard, A. Kenyon, and D. J. Thurman, “Epilepsy or seizure disorder? The effect of cultural and socioeconomic factors on self-reported prevalence,” Epilepsy Behav., vol. 62, pp. 214–217, Sep. 2016, doi: 10.1016/j.yebeh.2016.07.013.
• [2] A. W. Selassie, D. A. Wilson, G. U. Martz, G. G. Smith, J. L. Wagner, and B. B. Wannamaker, “Epilepsy beyond seizure: A population-based study of comorbidities,” Epilepsy Res., vol. 108, no. 2, pp. 305–315, Feb. 2014, doi: 10.1016/j.eplepsyres.2013.12.002.
• [3] M. M. Acharya, B. Hattiangady, and A. K. Shetty, “Progress in neuroprotective strategies for preventing epilepsy,” Progress in Neurobiology, vol. 84, no. 4. pp. 363–404, Apr. 2008, doi: 10.1016/j.pneurobio.2007.10.010.
• [4] C. Harden et al., “Practice guideline summary: Sudden unexpected death in epilepsy incidence rates and risk factors: Report of the guideline development, dissemination, and implementation subcommittee of the American Academy of Neurology and the American Epilepsy Society,” Epilepsy Curr., vol. 17, no. 3, pp. 180–187, May 2017, doi: 10.5698/1535-7511.17.3.180.
• [5] P. Ichai et al., “Fulminant hepatitis after grand mal seizures: Mechanisms and role of liver transplantation,” Hepatology, vol. 38, no. 2, pp. 443–451, Aug. 2003, doi: 10.1053/jhep.2003.50327.
• [6] A. Ahmet and S. Bilal, “Evaluation of Oxidative Stress Parameters in Liver in Pentylenetetrazole - Induced Acute and Chronic Epilepsy Model in Rats,” Am J Biomed Sci Res, no. 6, pp. 2019–2024, doi: 10.34297/AJBSR.2019.05.000966.
• [7] Vercueil. L, “John Libbey Eurotext - Epileptic Disorders - Epilepsy and neurodegenerative diseases in adults: a clinical review,” 2006. https://www.jle.com/fr/revues/epd/e-docs/epilepsy_and_neurodegenerative_diseases_in_adults_a_clinical_review_269372/article.phtml (accessed Feb. 20, 2020).
• [8] K. M. Nau, G. D. Divertie, A. K. Valentino, and W. D. Freeman, “Safety and efficacy of levetiracetam for critically Ill patients with seizures,” Neurocrit. Care, vol. 11, no. 1, pp. 34–37, Aug. 2009, doi: 10.1007/s12028-009-9185-0.
• [9] S. H. Akbas, A. Yegin, and T. Ozben, “Effect of pentylenetetrazol-induced epileptic seizure on the antioxidant enzyme activities, glutathione and lipid peroxidation levels in rat erythrocytes and liver tissues,” Clin. Biochem., vol. 38, no. 11, pp. 1009–1014, Nov. 2005, doi: 10.1016/j.clinbiochem.2005.07.012.
• [10] H. Tilg and A. M. Diehl, “Cytokines in alcoholic and nonalcoholic steatohepatitis,” New England Journal of Medicine, vol. 343, no. 20. pp. 1467–1467, Nov. 16, 2000, doi: 10.1056/NEJM200011163432007.
• [11] D. A. West et al., “Role for tumor necrosis factor α receptor 1 and interleukin-1 receptor in the suppression of mouse hepatocyte apoptosis by the peroxisome proliferator nafenopin,” Hepatology, vol. 30, no. 6, pp. 1417–1424, Dec. 1999, doi: 10.1002/hep.510300612.
• [12] P. Akerman et al., “Antibodies to tumor necrosis factor-α inhibit liver regeneration after partial hepatectomy,” Am. J. Physiol. - Gastrointest. Liver Physiol., vol. 263, no. 4 26-4, 1992, doi: 10.1152/ajpgi.1992.263.4.g579.