Table 2.
Experimental studies showing beneficial effects of GT and its ingredients on anterior segmentocular diseases.
| type of study | cell type/animal model | target disease | intervention | results | reference |
|---|---|---|---|---|---|
| in-vivo | mice | dry eye disease | topical 0.01% and 0.1% EGCG | Administering EGCG topically can alleviate the clinical and inflammatory symptoms of DED by suppressing cytokine expression and CD11b + cell infiltration in the cornea. | [62] |
| in-vitro | human primary pterygium | pterygium | GTE(16.25 μg/mL) and EGCG (25 μM) | GTE and EGCG had a mitigating effect on the survival and movement of primary pterygium cells in vitro, without causing any harm to conjunctival cells. This discovery presents a new and innovative approach to treating primary pterygium. | [71] |
| in-vitro | human corneal fibroblasts | corneal ulcer | EGCG (10, 30, 100 and 300 μM) | EGCG suppresses the degradation of collagen by corneal fibroblasts that have been induced by IL-1b, possibly by impeding the upregulation of uPA, the conversion of plasminogen to plasmin through uPA, and the activation of pro-MMP1 by plasmin. As a result, EGCG requires additional research as a potential therapy for corneal ulcer. | [76] |
| in-vivo | rat | glaucoma | EGCG (50 mg/kg/day) | The NF-κB signaling pathway is involved in the anti-inflammatory impact of EGCG. | [85] |
| in-vivo | rat retinal ganglion cells | glaucoma | GTE (275 mg/kg) | To summarize, under ischemic conditions, GTE provides neuroprotection to retinal ganglion cells, which proposes a prospective therapeutic approach for the treatment of glaucoma and optic neuropathies. | [88] |
| in-vivo | mice | glaucomatous optic neuropathy (GON) | EGCG (50 mg/kg/day) | The results indicate that the intake of EGCG has a neuroprotective effect on retinal ganglion cells (RGCs) in a mouse model of increased intraocular pressure (IOP). | [87] |
| in-vitro | human trabecular meshwork (HTM) cell | primary open-angle glaucoma | EGCG (10, 20, 40, and 80 μM) | EGCG can shield TM cells from endoplasmic reticulum stress, indicating that it has the potential as a therapeutic choice for treating POAG. | [90] |
| in-vivo | rat | uveitis | GTE (550 mg/kg) | GTE is a powerful anti-inflammatory agent that effectively combats endotoxin-induced uveitis (EIU) inflammation, indicating its potential usefulness in treating acute uveitis. | [97] |
| in-vivo | murine | autoimmune uveitis | GTE (137.5 mg/kg and 275 mg/kg GTE suspension, 96.25 mg/kg and 192.5 mg/kg EGCG suspension in 0.1 mL distilled water) | Relief from intraocular inflammation can be achieved by suppressing the expression of pro-inflammatory genes associated with Th17 cells. | [99] |
| in-vivo | rat | uveitis | GTE (550 mg/kg) | The anti-inflammatory effects of a substance on ocular inflammation induced by endotoxin. | [98] |
| in-vivo | rat | uveitis | GTE (550 mg/kg), catechins mixtures, EGCG (375.2 mg/kg) | The combination of GTE and its catechins demonstrated a strong anti-inflammatory effect in a laboratory model of acute ocular inflammation. | [156] |
| in-vitro | αA-crystallin Peptide | cataract | EGCG (1, 5 and 50 mM) | EGCG effectively inhibits the concentration-dependent aggregation of αA (66–80) peptide. Additionally, it can also break up pre-existing aggregates of αA (66–80). This research indicates that EGCG may have the potential to prevent cataract formation and aid in the reversal of the disease. | [111] |
| in-vitro &docking study | human γB-crystallin | cataract | EGCG (4, 8, 10, 12, 16, 20, 30 and 40 μM) | EGCG has the capability to safeguard human γB-crystallin from photodamage induced by oxidative stress. | [157] |
| in-vitro & docking study | human γ-crystallin protein | cataract | EGCG (4, 8, 12 and 16 μM) | EGCG inhibits tryptophan oxidation of human γ-crystallin in cataractous ocular lenses in the presence of H2O2. | [158] |
| in-vitro &molecular dynamics study | human γB-crystallin protein | cataract | EGCG (2 mg/mL) | EGCG has inhibitory potency against the aggregation of human γB-crystallin at high temperatures and low pH. | [110] |
| in-vitro | human lens epithelial (HLE) cells | cataract | EGCG (10, 25, 50, 75, 100and 150 μM) | These discoveries imply that EGCG guards HLE cells against H2O2-induced apoptosis mediated by mitochondria, via the regulation of caspases, the Bcl-2 family, and the MAPK and Akt pathways. | [112] |
OSD - Ocular Surface Diseases.
DED - Dry Eye Disease.
EGCG - Epigallocatechin Gallate.
IL-1b - Interleukin-1 beta.
GTE - Green Tea Extract.
POAG - Primary Open-Angle Glaucoma.
TM - Trabecular Meshwork.
NF-κB - Nuclear Factor-kappa B.
RGCs - Retinal Ganglion Cells.
IOP - Intraocular Pressure.
H2O2 - Hydrogen Peroxide.