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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Hindsiipropane B inhibits HIV-1 Tat-induced inflammatory responses by suppressing HDAC6-NADPH oxidase-ROS-MAPK-NF-リB/AP-1 axis in astrocytes
Hyundong Jo1, Ha Young Jang2, Gi Soo Youn1, Donggyu Kim1, Chae Yeon Lee1, Jae Hee Jang1, Soo Young Choi1, Jong-Gab Jun2, Jinseu Park1,*
1Department of Biomedical Science and 2Department of Chemistry, Hallym University
Human immunodeficiency virus-1 (HIV-1) transactivator of transcription (Tat) is an important viral factor in neuro-inflammation. Hindsiipropane B, present in Celastrus hindsii, possesses various biological mechanisms including anti-inflammatory activity. In this report, we explored the regulatory activity of hindsiipropane B on HIV-1 Tat-mediated chemokine production and its mode of action in astrocytes. Hindsiipropane B significantly alleviated HIV-1 Tat-mediated production of inflammatory chemokines, CCL2, CXCL8, and CXCL10. Hindsiipropane B inhibited expression of HDAC6, which is important regulator in HIV-1 Tat-mediated chemokine production. Hindsiipropane B diminished HIV-1 Tat-mediated reactive oxygen species (ROS) generation and NADPH oxidase activation/expression. Furthermore, hindsiipropane B inhibited HIV-1 Tat-mediated signaling cascades including MAPK, NF-リB, and AP-1. These data suggest that hindsiipropane B exerts its inhibitory effects on HIV-1 Tat-mediated chemokine production via down-regulating the HDAC6-NADPH oxidase-MAPK-NF-リB/AP-1 signaling axis, and could serve as a therapeutic lead compound against HIV-1 Tat-associated neuro-inflammation.
Abstract, Accepted Manuscript(in press) [Submitted on March 23, 2018, Accepted on April 23, 2018]
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