Search

Objective. To investigate the role of nestin in regulating Keap1-nuclear factor erythroid-2-related factor 2 (Nrf2)-heme oxygenase-1-(HO-1-) mediated antioxidant responses in stress and malignant hematopoiesis. Methods. The mRNA of peripheral blood mononuclear cells was extracted from 20 leukemia patients and 20 healthy people who were hospitalized in the Hematology Department of our hospital from September 2020 to December 2021, and the mRNA levels of nestin, Keap1, Nrf2, and HO-1 were detected by real-time- (RT-) PCR. Results. Compared with healthy controls, the mRNA of nestin, Keap1, Nrf2, and HO-1 in peripheral blood mononuclear cells of leukemia patients was significantly upregulated. Conclusion. The occurrence and development of leukemia are closely related to nestin regulating Keap1-Nrf2-Ho-1 signal pathway. Research Significance. This study determined the effect of nestin on the biological behavior of leukemia cells and its possible mechanism and confirmed that nestin may be a marker of tumor and tumor blood vessels. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) can induce intestinal inflammatory response and mucosal injury. Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to prevent oxidative stress and inflammatory response in gut after TBI. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), an Nrf2 inducer, can protect against TBI-induced intestinal inflammatory response andmucosal injury in mice. Adult male ICR mice were randomly divided into three groups: (1) sham + vehicle group, (2) TBI + vehicle group, and (3) TBI + tBHQ group (n = 12 per group). Closed head injury was adopted using Hall's weight-dropping method. Intestinal mucosa apoptosis and inflammatory- related factors, such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α(TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), were investigated at 24 h after TBI. As a result, we found that oral treatment with 1% tBHQ prior to TBI for one week markedly decreased NF-κB activation, inflammatory cytokines production, and ICAM-1 expression in the gut. Administration of tBHQ also significantly attenuated TBI-induced intestinalmucosal apoptosis. The results of the present study suggest that tBHQ administration could suppress the intestinal inflammation and reduce the mucosal damage following TBI. [ABSTRACT FROM AUTHOR]