Jingjuan Huang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jingjuan Huang has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Bing Liu
Guangzhou Key Laboratory of Construction and Application of New Drug Screening Model Systems, Guangdong Pharmaceutical University, Guangzhou 510006, China
2 shared publications - Jia Fu
School of Nursing, Guangdong Pharmaceutical University, Guangzhou 510006, China
2 shared publications - Rui Wang
School of Nursing, Guangdong Pharmaceutical University, Guangzhou, China
2 shared publications - Tianhui You
School of Nursing, Guangdong Pharmaceutical University, Guangzhou 510006, China
2 shared publications Lin Zhang
Operating Room, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China
1 shared publicationQimei Liang
Operating Room, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China
1 shared publication
Latest Publications
- Open Access
- 9 March 2026
- Published by Springer Nature in BMC Nursing
- Vol. 25 (1)
The effects of the forgetting curve in the training of knee arthroplasty surgical instrument nurses: a pilot randomized controlled trial
This study aimed to compare the conventional review teaching method with the forgetting curve-based teaching method in the training of novice knee replacem
- 9 March 2026
- Published by Springer Nature in BMC Nursing
- Vol. 25 (1)
Open AccessThe effects of the forgetting curve in the training of knee arthroplasty surgical instrument nurses: a pilot randomized controlled trial
This study aimed to compare the conventional review teaching method with the forgetting curve-based teaching method in the training of novice knee replacem
- Open Access
A Synthetic Curcuminoid Analog, (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone, Ameliorates Impaired Wound Healing in Streptozotocin-Induced Diabetic Mice by Increasing miR-146a
The impairment in diabetic wound healing represents a significant clinical problem, with no efficient targeted treatments for these wound disorders. Curcumin is well confirmed to improve diabetic wound healing, however, its low bioavailability and poor solubility severely limit its clinical application. This study aims to provide the pharmacological basis for the use of (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone (C66). The results showed that topically applied C66 improved cutaneous wound healing in vivo. Further studies showed that C66 treatment increased the level of microRNA-146a (miR-146a) in the wounds in streptozotocin (STZ)-induced diabetic mice, downregulated the expression of interleukin-1 receptor-associated kinase 1 (IRAK1) and phosphorylated nuclear factor-κB (NF-κB) p65 subunit (p-p65) (both p < 0.05), and suppressed the mRNA expression of inflammation-related cytokines, tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and interleukin-6 (IL-6). The in vitro data obtained in human umbilical vein endothelial cells (HUVECs) showed that C66 could reverse high glucose (HG)-induced NF-κB activation due to upregulation of miR-146a expression, which matched the in vivo findings. In conclusion, the present study indicates that C66 exerts anti-inflammation activity and accelerates skin wound healing of diabetic mice, probably via increasing miR-146a and inhibiting the NF-κB-mediated inflammation pathway. Therefore, C66 may be a promising alternative for the treatment of diabetic wounds.
Open AccessA Synthetic Curcuminoid Analog, (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone, Ameliorates Impaired Wound Healing in Streptozotocin-Induced Diabetic Mice by Increasing miR-146a
The impairment in diabetic wound healing represents a significant clinical problem, with no efficient targeted treatments for these wound disorders. Curcumin is well confirmed to improve diabetic wound healing, however, its low bioavailability and poor solubility severely limit its clinical application. This study aims to provide the pharmacological basis for the use of (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone (C66). The results showed that topically applied C66 improved cutaneous wound healing in vivo. Further studies showed that C66 treatment increased the level of microRNA-146a (miR-146a) in the wounds in streptozotocin (STZ)-induced diabetic mice, downregulated the expression of interleukin-1 receptor-associated kinase 1 (IRAK1) and phosphorylated nuclear factor-κB (NF-κB) p65 subunit (p-p65) (both p < 0.05), and suppressed the mRNA expression of inflammation-related cytokines, tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and interleukin-6 (IL-6). The in vitro data obtained in human umbilical vein endothelial cells (HUVECs) showed that C66 could reverse high glucose (HG)-induced NF-κB activation due to upregulation of miR-146a expression, which matched the in vivo findings. In conclusion, the present study indicates that C66 exerts anti-inflammation activity and accelerates skin wound healing of diabetic mice, probably via increasing miR-146a and inhibiting the NF-κB-mediated inflammation pathway. Therefore, C66 may be a promising alternative for the treatment of diabetic wounds.