AIM: To explore the role of nuclear factor erythroid 2-related factor 2 (Nrf2) in traumatic brain injury (TBI)-induced intestinal inflammatory response and gut barrier dysfunction in the mice. METHODS: Wild-type Nrf2 (+/+) and Nrf2 (-/-)-deficient mice were subjected to a moderately severe weight-drop impact-acceleration head injury. We measured nuclear factor kappa B (NF-kappaB) by electrophoretic mobility shift assay (EMSA); tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) by enzyme-linked immunosorbent assay (ELISA); intercellular adhesion molecule-1 (ICAM-1) by immunohistochemistry; intestinal permeability by lactulose/mannitol (L/M) test; plasma endotoxin by chromogenic limulus amebocyte lysate test. RESULTS: Intestinal levels of NF-kappaB, pro-inflammatory cytokines and ICAM-1 in Nrf2 (-/-)-deficient mice were significantly higher compared with Nrf2 (+/+) mice at 24h after TBI. Furthermore, higher intestinal permeability and plasma level of endotoxin were observed in the Nrf2 (-/-) mice compared with Nrf2 (+/+) mice. CONCLUSION: Nrf2 plays an important protective role in limiting intestinal inflammatory response and gut barrier dysfunction after TBI.
AIM: To explore the role of nuclear factor erythroid 2-related factor 2 (Nrf2) in traumatic brain injury (TBI)-induced intestinal inflammatory response and gut barrier dysfunction in the mice. METHODS: Wild-type Nrf2 (+/+) and Nrf2 (-/-)-deficient mice were subjected to a moderately severe weight-drop impact-acceleration head injury. We measured nuclear factor kappa B (NF-kappaB) by electrophoretic mobility shift assay (EMSA); tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) by enzyme-linked immunosorbent assay (ELISA); intercellular adhesion molecule-1 (ICAM-1) by immunohistochemistry; intestinal permeability by lactulose/mannitol (L/M) test; plasma endotoxin by chromogenic limulus amebocyte lysate test. RESULTS: Intestinal levels of NF-kappaB, pro-inflammatory cytokines and ICAM-1 in Nrf2 (-/-)-deficient mice were significantly higher compared with Nrf2 (+/+) mice at 24h after TBI. Furthermore, higher intestinal permeability and plasma level of endotoxin were observed in the Nrf2 (-/-) mice compared with Nrf2 (+/+) mice. CONCLUSION:Nrf2 plays an important protective role in limiting intestinal inflammatory response and gut barrier dysfunction after TBI.
Authors: Rana Al-Sadi; Shuhong Guo; Dongmei Ye; Karol Dokladny; Tarik Alhmoud; Lisa Ereifej; Hamid M Said; Thomas Y Ma Journal: J Immunol Date: 2013-05-08 Impact factor: 5.422
Authors: M Tohidnezhad; D Varoga; C J Wruck; L O Brandenburg; A Seekamp; M Shakibaei; T T Sönmez; Thomas Pufe; S Lippross Journal: Histochem Cell Biol Date: 2011-04-08 Impact factor: 4.304
Authors: Laura M Cox; Hadi Abou-El-Hassan; Amir Hadi Maghzi; Julia Vincentini; Howard L Weiner Journal: Brain Res Date: 2019-08-13 Impact factor: 3.252