Efek Pemberian Ekstrak Rimpang Kunyit (Curcuma longa) Terhadap Chronic Traumatic Encephalopathy pada Rattus Novergicus Galur Sprague Dawley

Abstract

Pendahuluan. Cedera kepala berulang akan menyebabkan Chronic Traumatic Encephalopathy (CTE), suatu degenerasi saraf dini yang ditandai dengan penumpukan protein tau patologis, transactive response-DNA binding protein of 43 kDa (TDP-43), dan amyloid beta. Neuroinflamasi, terutama aktivasi mikroglia, memegang peranan pada penumpukan protein tau. Ekstrak kunyit sudah sejak dahulu diketahui berperan sebagai antiinflamasi kuat dan sudah terbukti efektif pada penyakit degenerasi saraf lainnya, seperti penyakit Alzheimer. Tujuan penelitian ini adalah membuktikan peranan ekstrak kunyit pada CTE melalui penghambatan neuroinflamasi. Metode. Ini merupakan penelitian eksperimental murni dengan disain post-test. Pada tikus Sprague-dawley jantan dengan berat 300-500 gram, diberikan perlakuan trauma dan pemberian ekstrak kunyit. Trauma dilakukan dengan menjatuhkan beban seberat 40 gram dari ketinggian 1 meter ke atas verteks tikus. Trauma dilakukan dengan frekuensi total 12 kali, terbagi ke dalam 4 hari (0, 1, 3, dan 7), dengan perincian tiga kali trauma setiap harinya. Ekstrak kunyit diberikan peroral setiap harinya dengan dosis 500 mg/kgBB. Berdasarkan perlakuan, kelompok dibagi tiga yaitu perlakuan 1 (pemberian ekstrak bersamaan dengan trauma selama satu minggu), perlakuan 2 (pemberian ekstrak setelah trauma) dan perlakuan 3 (pemberian ekstrak sebelum perlakuan trauma). Diagnosis CTE dikonfirmasi berdasarkan ekspresi protein tau terfosforilasi (AT-8), TDP-43, dan amyloid beta. Sementara itu, neuroinflamasi dikonfirmasi dengan penanda aktivasi microglia (CD-68) dan penanda astrogliosis (GFAP). Hasil. Perlakuan trauma meningkatkan ekspresi AT-8, TDP-43, amyloid beta, CD-68, dan GFAP secara signifikan. Sementara itu, pemberian ekstrak kunyit menyebabkan penurunan signifikan ekspresi parameter-parameter tersebut. Penurunan paling signifikan terjadi pada kelompok yang mendapatkan ekstra kunyit sebelum trauma dilakukan Simpulan. Ekstrak kunyit memiliki potensi sebagai pilihan terapi pada CTE melalui penghambatan neuroinflamasi. Meskipun demikian, peranan ekstrak kunyit lebih terlihat sebagai neuroprotektor dibandingkan efek kuratif saja.

Introduction. Repetitive head injury will be resulted in chronic traumatic encephalopathy (CTE), that is an early progressive neurodegenerative changes marked by deposition of pathologic tau protein, transactive response-DNA binding protein of 43 kDa (TDP-43), and beta amyloid. Neuroinflammation, especially microglial activation, is known to have significant role in the deposition of pathologic tau protein. Turmeric extract (TE) is potent anti-inflammatory agent and is proved to be effective in other neurodegerative disease, such as Alzheimer’s disease. The aim of this study was to explore the potency of turmeric extract on CTE by inhibiting neuroinflammation. Methods. This was a true experimental study with post-test only control group design. Male Sprague-dawley rats, weighing 300-500 grams, received repetitive head injury and turmeric supplementation. A 40-gram mass was dropped into the vertex from 1 metre height three times daily on day 0,1,3,7, with total frequency 12 times. TE supplementation was given daily, 500 mg/kg orally. Based on this, treatment group were divided into three groups. Subjects in first group had trauma along TE supplementation in one week. In the second group, TE supplementation was started one day after the last trauma for one weeks. The third group was pretreatment group. TE supplementation was started one week before trauma protocol. In this group, TE supplementation was also given along the trauma for the next one week. CTE was confirmed by expression of phosphorylated tau protein (AT-8), TDP-43, and amyloid beta. Meanwhile, neuroinflammation was confirmed with microglial activation marker (CD-68) and astrogliosis marker (GFAP). Result. Repetitive head injury increased the expression of AT-8, TDP-43, beta amyloid significantly. There was also increased in the expression of GFAP and CD-68. TE supplementation decreased the expression of all CTE markers as well as the neuroinflammation markers significantly. The most notable reduction was seen on pretreatment group. Conclusion. TE supplementation had potency as a treatment modality in CTE by inhibiting neuroinflammation. Rather as a curative agent, TE supplementation might have role as a neuroprotective agent.