Chao-Chiang Tu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Chao-Chiang Tu has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Chao-Hsien Sung
Division of Anesthesiology, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei City, Taiwan
1 shared publication - Chia-Chi Kung
Division of Anesthesiology, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei City 24352, Taiwan
1 shared publication - Chih-Li Chen
School of Medicine, College of Medicine, Fu Jen Catholic University, No. 510 Zhongzheng Rd., Xinzhuang Dist., New Taipei 24205, Taiwan
1 shared publication - Chun-Hsien Fu
Department of Anesthesiology, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei 24352, Taiwan
1 shared publication - Jen-Hao Liu
Department of Anesthesiology, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei 24352, Taiwan
1 shared publication - Po-Heng Chen
School of Medicine, College of Medicine, Fu Jen Catholic University, No. 510 Zhongzheng Rd., Xinzhuang Dist., New Taipei 24205, Taiwan
1 shared publication
Latest Publications
- Open Access
- 28 March 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (7) , 3096
CLARIX FLO Inhibits DRG Adhesion-Induced Neuropathic Pain Through the CD44–TRPV1 Signaling Pathway
DRG adhesion is a key pathological feature of failed back surgery syndrome and a major cause of neuropathic pain. DRG, or epidural adhesion, commonly results from spinal surgery, leakage of disk material into the epidural space, or inflammation. To better mimic this clinical condition, we developed a novel and reliable animal model of DRG adhesion-induced neuropathic pain. Using this model, we investigated the therapeutic potential and underlying mechanisms of CLARIX FLO, a sterile, particulate human amniotic membrane and umbilical cord tissue product. Our results demonstrate that CLARIX FLO exerts significant analgesic and anti-inflammatory effects in the DRG adhesion model. The application of CLARIX FLO to the injured DRG markedly attenuated mechanical allodynia. CLARIX FLO treatment also reduced outer sheath thickening, suppressed the inflammatory microenvironment, and decreased hypersensitivity of isolectin B4-positive neurons. Mechanistically, CD44 was identified as a potential downstream mediator of CLARIX FLO. Furthermore, a high dose of HC-HA/PTX3, the key bioactive component of CLARIX FLO, effectively reversed mechanical allodynia and inflammation. Notably, CLARIX FLO inhibited the overexpression of TNF-α and TRPV1 adhering to the DRG. In this study, we demonstrated that CLARIX FLO effectively alleviates DRG adhesion-induced neuropathic pain through a CD44–TRPV1-dependent mechanism.
- 28 March 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (7) , 3096
Open AccessCLARIX FLO Inhibits DRG Adhesion-Induced Neuropathic Pain Through the CD44–TRPV1 Signaling Pathway
DRG adhesion is a key pathological feature of failed back surgery syndrome and a major cause of neuropathic pain. DRG, or epidural adhesion, commonly results from spinal surgery, leakage of disk material into the epidural space, or inflammation. To better mimic this clinical condition, we developed a novel and reliable animal model of DRG adhesion-induced neuropathic pain. Using this model, we investigated the therapeutic potential and underlying mechanisms of CLARIX FLO, a sterile, particulate human amniotic membrane and umbilical cord tissue product. Our results demonstrate that CLARIX FLO exerts significant analgesic and anti-inflammatory effects in the DRG adhesion model. The application of CLARIX FLO to the injured DRG markedly attenuated mechanical allodynia. CLARIX FLO treatment also reduced outer sheath thickening, suppressed the inflammatory microenvironment, and decreased hypersensitivity of isolectin B4-positive neurons. Mechanistically, CD44 was identified as a potential downstream mediator of CLARIX FLO. Furthermore, a high dose of HC-HA/PTX3, the key bioactive component of CLARIX FLO, effectively reversed mechanical allodynia and inflammation. Notably, CLARIX FLO inhibited the overexpression of TNF-α and TRPV1 adhering to the DRG. In this study, we demonstrated that CLARIX FLO effectively alleviates DRG adhesion-induced neuropathic pain through a CD44–TRPV1-dependent mechanism.