Oral coral-like resveratrol nanocomplex reduces dry eye disease signs in animal models via ocular and systemic redox homeostasis
In murine models of dry eye disease (DED), an oral resveratrol nanocomplex (RES-DG-NC) reduced ocular inflammatory and oxidative stress markers compared to free resveratrol and vehicle — a favorable direction confined entirely to preclinical data with no human evidence.
| Population | Experimentally induced DED murine models (no human participants) |
|---|---|
| Intervention | Oral coral-like resveratrol nanocomplex (RES-DG-NC) |
| Comparator | Free oral resveratrol, vehicle (DG-NC without RES), and untreated control |
| Outcome | Oral bioavailability of resveratrol (AUC/Cmax); Ocular reactive oxygen species (ROS); Ocular superoxide dismutase (SOD) activity; Ocular malondialdehyde (MDA); Ocular and systemic inflammatory cytokines (IL-1β, TNF-α, IL-6); Ocular surface integrity (fluorescein score); Conjunctival goblet cell density |
Summary of findings
| Outcome | Effect | 95% CI | Certainty | Clinical relevance | Notes |
|---|---|---|---|---|---|
| Oral bioavailability of resveratrol (AUC/Cmax) | Increased AUC and Cmax vs free RES; exact values and 95% CI not recoverable from truncated text | — | Very low | — | 1 studies |
| Ocular reactive oxygen species (ROS) | Reduced vs control and free RES; exact values and 95% CI not recoverable from truncated text | — | Very low | — | 1 studies |
| Ocular superoxide dismutase (SOD) activity | Increased vs control; exact values and 95% CI not recoverable from truncated text | — | Very low | — | 1 studies |
| Ocular malondialdehyde (MDA) | Reduced vs control; exact values and 95% CI not recoverable from truncated text | — | Very low | — | 1 studies |
| Ocular and systemic inflammatory cytokines (IL-1β, TNF-α, IL-6) | Reduced vs control and free RES; exact values and 95% CI not recoverable from truncated text | — | Very low | — | 1 studies |
| Ocular surface integrity (fluorescein score) | Improved vs control; exact values and 95% CI not recoverable from truncated text | — | Very low | — | 1 studies |
| Conjunctival goblet cell density | Improved vs control; exact values and 95% CI not recoverable from truncated text | — | Very low | — | 1 studies |
Context
DED affects hundreds of millions worldwide; current topical therapies carry long-term adverse effects. Oral resveratrol is constrained by poor bioavailability. This study tests whether a dipotassium glycyrrhizinate (DG)-based nanocrystal formulation overcomes this pharmacokinetic barrier in animal models.
What the study showed
RES-DG-NC improved oral bioavailability of resveratrol versus free RES (absolute AUC and Cmax values not recoverable from the truncated text). In murine DED models, the formulation reduced ocular ROS, increased SOD activity, and reduced MDA in ocular tissues versus controls; it also reduced IL-1β, TNF-α, and IL-6 locally and systemically. Ocular surface integrity (fluorescein score and goblet cell density) improved relative to control groups. Specific 95% CI and p-values were not recoverable from the provided text.
How it was done
Preclinical study combining in vitro experiments (human corneal epithelial cells under oxidative stress) and in vivo murine DED models. The nanoformulation combines resveratrol, DG, and nanocrystals with a coral-like structure. Exact group sizes and full experimental duration were not recoverable from the truncated text provided.
Effect magnitude
Effect sizes with 95% CI were not recoverable from the truncated text; the study reports statistically significant differences in redox and inflammatory markers favoring RES-DG-NC over free RES and controls, without accessible absolute quantification in this analysis.
Risk of bias
Entirely preclinical study (in vitro + animal); no human data. The provided text is truncated, preventing recovery of exact sample sizes, 95% CI values, risk of bias assessment tools (RoB 2 or ROBINS-I not mentioned), and complete protocols. Murine DED models have limited translational validity for multifactorial human disease.
What this study does NOT prove
This study does not prove efficacy or safety in humans with DED. It does not establish causality between oral systemic redox homeostasis and clinical dry eye improvement in human populations.
In clinical practice
No clinical practice change is supported by this study. Clinicians should not recommend this formulation to patients; it has not been tested in humans. The study identifies a candidate for phase I/II clinical trials.
Limitations
Entirely preclinical study (in vitro + animal); no human data. The provided text is truncated, preventing recovery of exact sample sizes, 95% CI values, risk of bias assessment tools (RoB 2 or ROBINS-I not mentioned), and complete protocols. Murine DED models have limited translational validity for multifactorial human disease.
What is still missing
Clinical trials in humans with confirmed DED are required to establish safety, pharmacokinetics, and clinical efficacy. Long-term dose-response and safety studies in animals also precede any clinical translation.
Technical appendix
Version history
- 1.0 · 2026-09-15 — Auto-generated under Evidence Standard v1.0