TY  - GEN
AB  - Atopic dermatitis (AD) poses a significant global health challenge, characterized by dysregulated inflammation and apoptotic processes. This study explores the therapeutic efficacy of hinokitiol, employing a comprehensive in vivo and in vitro approach. Assessment of inflammation-related markers in the animal model included observation of physical appearance, Western blotting, ELISA, and H&E staining. Additionally, the cell culture model enabled the evaluation of apoptosis and ROS levels using MTT assay, crystal violet staining, Western blot, and DCFDA assays. The results revealed hinokitiol's proficiency in ameliorating ear and skin morphology in the DNCB-induced AD model, mediated through the TLR4/MyD88 pathway. Notably, hinokitiol intervention led to a reduction in both M1 and M2 macrophage phenotypes. In vitro investigations demonstrated hinokitiol's ability to enhance cell viability and morphology under TNF-α and IFN-γ induction. Mechanistically, hinokitiol exhibited regulatory effects on apoptosis-related proteins, including Bax, Cytochrome c, Caspase-3, and PARP, thereby averting cellular damage. These findings suggest that hinokitiol is a promising natural compound with significant potential for alleviating inflammation and apoptosis in AD, indicating potential avenues for future therapeutic developments.
AD  - Taipei Medical University
AD  - Taipei Medical University
AD  - Taipei Medical University
AD  - Taipei Medical University
AD  - University of Chicago
AD  - Taipei Medical University
AU  - Tai, Ling-Ray
AU  - Chiang, Yi-Fen
AU  - Huang, Ko-Chieh
AU  - Chen, Hsin-Yuan
AU  - Ali, Mohamed
AU  - Hsia, Shih-Min
DA  - 2023-12-20
ID  - 10498
JF  - Biomedicine & Pharmacotherapy
KW  - Atopic dermatitis
KW  - Inflammation
KW  - Apoptosis
KW  - Hinokitiol
L1  - https://knowledge.uchicago.edu/record/10498/files/Hinokitiol-as-a-modulator-of-TLR4-signaling-and-apoptotic-pathways-in-atopic-dermatitis.pdf
L2  - https://knowledge.uchicago.edu/record/10498/files/Hinokitiol-as-a-modulator-of-TLR4-signaling-and-apoptotic-pathways-in-atopic-dermatitis.pdf
L4  - https://knowledge.uchicago.edu/record/10498/files/Hinokitiol-as-a-modulator-of-TLR4-signaling-and-apoptotic-pathways-in-atopic-dermatitis.pdf
LA  - eng
LK  - https://knowledge.uchicago.edu/record/10498/files/Hinokitiol-as-a-modulator-of-TLR4-signaling-and-apoptotic-pathways-in-atopic-dermatitis.pdf
N2  - Atopic dermatitis (AD) poses a significant global health challenge, characterized by dysregulated inflammation and apoptotic processes. This study explores the therapeutic efficacy of hinokitiol, employing a comprehensive in vivo and in vitro approach. Assessment of inflammation-related markers in the animal model included observation of physical appearance, Western blotting, ELISA, and H&E staining. Additionally, the cell culture model enabled the evaluation of apoptosis and ROS levels using MTT assay, crystal violet staining, Western blot, and DCFDA assays. The results revealed hinokitiol's proficiency in ameliorating ear and skin morphology in the DNCB-induced AD model, mediated through the TLR4/MyD88 pathway. Notably, hinokitiol intervention led to a reduction in both M1 and M2 macrophage phenotypes. In vitro investigations demonstrated hinokitiol's ability to enhance cell viability and morphology under TNF-α and IFN-γ induction. Mechanistically, hinokitiol exhibited regulatory effects on apoptosis-related proteins, including Bax, Cytochrome c, Caspase-3, and PARP, thereby averting cellular damage. These findings suggest that hinokitiol is a promising natural compound with significant potential for alleviating inflammation and apoptosis in AD, indicating potential avenues for future therapeutic developments.
PY  - 2023-12-20
T1  - Hinokitiol as a modulator of TLR4 signaling and apoptotic pathways in atopic dermatitis
TI  - Hinokitiol as a modulator of TLR4 signaling and apoptotic pathways in atopic dermatitis
UR  - https://knowledge.uchicago.edu/record/10498/files/Hinokitiol-as-a-modulator-of-TLR4-signaling-and-apoptotic-pathways-in-atopic-dermatitis.pdf
Y1  - 2023-12-20
ER  -