Muhammad Faris (2020) Pengaruh Pemberian Acth4-10pro8gly9pro10 Terhadap Mediator Proinflamasi Tlr, Nf-Kb, Il-8, Tnf-Α, Dan Neutrofil Pada Jaringan Spinal Cord Yang Mengalami Cedera Kompresi Akut Studi Eksperimental pada Tikus Sprague-Dawley Model Spinal Cord Injur. Disertasi thesis, UNIVERSITAS AIRLANGGA.

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Abstract

Background: Acute spinal cord injury (SCI) is a devastating traumatic event often followed with decreased quality of life, making it as a significant public health burden. ACTH4-10PRO8-GLY9-PRO10 (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic analogue of a short ACTH fragment with augmented neuroactivity and known anti-inflammatory properties. Studies had shown intranasal administration of ACTH4-10 were able to reach the central nervous system with higher tissue concentration and longer duration compared to intravenous administration. Its effect on SCI model is postulated via melanocortin receptor but its direct mechanism still unknown. Methods: This experimental study was done on SCI model of Sprague-Dawley rat. TLR, NF-kB, IL-8, and TNF-α were observed using immunohistochemistry staining as inflammatory markers. Neutrophil was observed using Hematoxylin Eosin staining. Sham group for this study was done using normal saline. Spinal cord of rat model was observed on 3- and 6-hours following injury. Statistical analysis was done using ANOVA with Bonferoni correction for normal data distribution. Kruskal Wallis followed by non-parametric Mann-Whitney U test were used for abnormal data distribution. Result: TLR, NF-kB, IL-8, and TNF-α expression along with neutrophil count showed significant decrease on 3 hours and 6 hours observation in ACTH4-10 treated group compared to normal saline treated croup (p < 0,05). TLR-2, NF-kB, and IL-8 are able to be regulated in ACTH treated group down to control level showing no significant difference during 6 hours observation. Conclusion: ACTH4-10 intranasal administration significantly reduced inflammation cytokines expression of acute SCI animal model. It may supressed secondary tissue damage from inflammation cascade. ACTH4-10 might be beneficial in SCI cases to regulate over-expression of inflammation modulators.

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