Travmatik Beyin Hasarında İnflamatuvar Sitokinlerin Rolü

Travmatik beyin hasarı dünyada, 45 yaş altı bireylerde mortalite ve morbiditenin başlıca nedenlerinden biridir. Oluşan bu birincil lezyonlardan daha çok, esas olarak, bu direkt etkinin başlattığı ikincil süreç, mortalite ve morbiditeden sorumludur ve teröpatik müdahalelere de duyarlıdır. Birincil ve ikincil patofizyolojik süreçlerin her ikisi de hücresel mediatörlerin (proinflamatuvar sitokinler, prostaglandinler, serbest radikaller ve komplemanlar) salınımına, adezyon moleküllerinin ekspresyonuna, savunma ve glial hücrelerinin kemotaksisine ve transmigrasyonuna neden olmaktadır. Travmatik beyin hasarından sonra proinflamatuvar sitokinlerin üretimi ve sekresyonu hem insan hem de deneysel hayvan modellerinde gösterilmiştir. Beyinde travmadan sonra interlökin 1, interlökin 6, tümör nekroz faktör ve santral sinir sistemi kaynaklı sitokinlerin yüksek konsantrasyonlarda saptanması onların travmayı takiben gelişen patolojik süreçte önemli rol oynadıklarını düşündürmektedir. Bu sitokinlerinlerin hasar sürecinde oynadığı rolü bilmek ve geliştirilecek uygun ajanlar ile kendi kendine ilerleyici bu süreci bir noktada durdurmak yani nöronal hasarı azaltmak, kafa travmasında hayat kurtarıcı olabilir.

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Marmara Medical Journal-Cover
  • ISSN: 1019-1941
  • Yayın Aralığı: Yılda 3 Sayı
  • Başlangıç: 1988
  • Yayıncı: Marmara Üniversitesi