Yuan Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Yuan Li has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Chi-Wai Do
School of Optometry, The Hong Kong Polytechnic University, Hong Kong, China
1 shared publication - En Gao
PolyU–HuiKang Joint Laboratory, The Hong Kong Polytechnic University, Kowloon, Hong Kong
1 shared publication - Jingfang Bian
Centre for Myopia Research, School of Optometry, The Hong Kong Polytechnic University, Kowloon, Hong Kong
1 shared publication - Lingxiao Yi
Centre for Eye and Vision Research (CEVR), 17W Hong Kong, Science Park, Hong Kong
1 shared publication - Liping Zhou
Research Centre for Chinese Medicine Innovation (RCMI), The Hong Kong Polytechnic University, China
1 shared publication - Man-Sau Wong
State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen Research Institute of The Hong Kong Polytechnic University, Shenzhen 518057, China
1 shared publication
Latest Publications
- Open Access
- 20 October 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (20) , 9297
Recombinant Human Lysozyme Attenuates Hyperosmolarity-Induced Dry Eye Disease by Suppressing Oxidative Stress and Modulating NLRP3 Inflammasome Signaling
Given the escalating global prevalence of dry eye disease (DED) and the inadequacy of current palliative management, this study was to evaluate thetherapeutic potential of recombinant lysozyme (rlysozyme) and investigate underlying mechanisms. Human corneal epithelial cells (HCEC) were subjected to hyperosmotic stress and treated with graded rlysozyme. Cell viability, wound healing, barrier integrity, oxidative stress, cytokines, and mitochondrial function were evaluated by MTS and scratch assays, immunofluorescent staining, ELISA, qRT-PCR, and flow cytometry. Results: No cytotoxicity was observed at any of the tested concentrations (2.76 × 10−9–2.76 × 10−4 M) in HCEC. In hyperosmolarity-induced DED cells, rlysozyme at the highest concentrations (2.76 × 10−4 M) significantly increased cell viability by 12.30% (p < 0.001) and promoted corneal repair by 45.04% (p < 0.05), which were comparable to those of 0.4% hyaluronic acid (the positive control). It also improved via restoring ZO-1 organization. Mechanistically, qRT-PCR results revealed that rlysozyme reduced mRNA expression of IL-1β (by 28.7%), TNF (by 39.2%) and key NLRP3 inflammasome components, including NLRP3 (by 62.0%) and PYD and CARD domain-containing protein gene(PYCARD, 21.4%), while caspase-1 (CASP1) and IL-6 expression remained unchanged. Moreover, oxidative stress was attenuated, as evidenced by significant decreases in reactive oxygen species (ROS, by 59.1%), 8-hydroxy-2-deoxyguanosine levels (8-OHdG, by 23.6%) and total matrix metalloproteinase-9 (MMP-9, by 64.3%) protein levels (p < 0.001), while mitochondrial membrane potential was assessed qualitatively. In conclusion, this study demonstrates thatrlysozyme effectively enhanced corneal epithelial cell viability, promoted wound healing, and restored ZO-1 structural organization without inducing cytotoxicity. These protective effects were associated with downregulation of NLRP3 inflammasome-related genes and attenuation of oxidative stress, supporting further investigation of its therapeutic potential in DED.
- 20 October 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (20) , 9297
Open AccessRecombinant Human Lysozyme Attenuates Hyperosmolarity-Induced Dry Eye Disease by Suppressing Oxidative Stress and Modulating NLRP3 Inflammasome Signaling
Given the escalating global prevalence of dry eye disease (DED) and the inadequacy of current palliative management, this study was to evaluate thetherapeutic potential of recombinant lysozyme (rlysozyme) and investigate underlying mechanisms. Human corneal epithelial cells (HCEC) were subjected to hyperosmotic stress and treated with graded rlysozyme. Cell viability, wound healing, barrier integrity, oxidative stress, cytokines, and mitochondrial function were evaluated by MTS and scratch assays, immunofluorescent staining, ELISA, qRT-PCR, and flow cytometry. Results: No cytotoxicity was observed at any of the tested concentrations (2.76 × 10−9–2.76 × 10−4 M) in HCEC. In hyperosmolarity-induced DED cells, rlysozyme at the highest concentrations (2.76 × 10−4 M) significantly increased cell viability by 12.30% (p < 0.001) and promoted corneal repair by 45.04% (p < 0.05), which were comparable to those of 0.4% hyaluronic acid (the positive control). It also improved via restoring ZO-1 organization. Mechanistically, qRT-PCR results revealed that rlysozyme reduced mRNA expression of IL-1β (by 28.7%), TNF (by 39.2%) and key NLRP3 inflammasome components, including NLRP3 (by 62.0%) and PYD and CARD domain-containing protein gene(PYCARD, 21.4%), while caspase-1 (CASP1) and IL-6 expression remained unchanged. Moreover, oxidative stress was attenuated, as evidenced by significant decreases in reactive oxygen species (ROS, by 59.1%), 8-hydroxy-2-deoxyguanosine levels (8-OHdG, by 23.6%) and total matrix metalloproteinase-9 (MMP-9, by 64.3%) protein levels (p < 0.001), while mitochondrial membrane potential was assessed qualitatively. In conclusion, this study demonstrates thatrlysozyme effectively enhanced corneal epithelial cell viability, promoted wound healing, and restored ZO-1 structural organization without inducing cytotoxicity. These protective effects were associated with downregulation of NLRP3 inflammasome-related genes and attenuation of oxidative stress, supporting further investigation of its therapeutic potential in DED.