Chien‑Hao Wanga, Jai‑Sing Yangb, Chao‑Jung Chenc,d, San‑Hua Sua, Hsin‑Yuan Yua, Yu‑Ning Juanb, Yu‑Jen Chiue,f,g*, Tsung‑Jung Hoh,i*
aDepartment of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan, bDepartment of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan, cGraduate Institute of Integrated Medicine, China Medical University, Taichung, Taiwan, dDepartment of Medical Research, Proteomics Core Laboratory, China Medical University Hospital, Taichung, Taiwan, eDivision of Plastic and Reconstructive Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan, fDepartment of Surgery, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, gInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, hIntegration Center of Traditional Chinese and Modern Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan, iSchool of Post‑Baccalaureate Chinese Medicine, Tzu Chi University, Hualien, Taiwan
Open Access funded by Buddhist Compassion Relief Tzu Chi Foundation
Abstract
Objectives: The protective effects and related mechanisms of Jing‑Si herbal tea (JSHT) were investigated in cellular damage mediated by pro‑inflammatory cytokines, including interleukin (IL)‑1β, IL‑6, and tumor necrosis factor‑α, on normal human lung fibroblast by multiomic platform analysis. Materials and Methods: The in silico high‑throughput target was analyzed using pharmacophore models by BIOVIA Discovery Studio 2022 with ingenuity pathway analysis software. To assess cell viability, the study utilized the MTT assay technique. In addition, the IncuCyte S3 ZOOM System was implemented for the continuous monitoring of cell confluence of JSHT‑treated cytokine‑injured HEL 299 cells. Cytokine concentrations were determined using a Quantibody Human Inflammation Array. Gene expression and signaling pathways were determined using next‑generation sequencing. Results: In silico high‑throughput target analysis of JSHT revealed ingenuity in canonical pathways and their networks. Glucocorticoid receptor signaling is a potential signaling of JSHT. The results revealed protective effects against the inflammatory cytokines on JSHT‑treated HEL 299 cells. Transcriptome and network analyses revealed that induction of helper T lymphocytes, TNFSF12, NFKB1‑mediated relaxin signaling, and G‑protein coupled receptor signaling play important roles in immune regulatory on JSHT‑treated cytokine‑injured HEL 299 cells. Conclusion: The findings from our research indicate that JSHT holds promise as a therapeutic agent, potentially offering advantageous outcomes in treating virus infections through various mechanisms. Furthermore, the primary bioactive components in JSHT justify extended research in antiviral drug development, especially in the context of addressing coronavirus.
Keywords: Coronavirus, Cytokines, Lung injury, Multiomic, Protective effects
