Inhibitory effects of water chestnut (Trapa bispinosa Roxb.) extract plus lutein on the progression of cataract and their impact on the retina and aorta in diabetic rats

TL;DR

A combination of water chestnut extract and lutein may slow cataract progression in diabetic rats by boosting antioxidants.

Contribution

This study is the first to simultaneously evaluate oxidative stress and antioxidant factors in diabetic cataract suppression using TBE plus lutein.

Findings

TBE plus lutein suppressed diabetic cataract progression in SDT rats.

Antioxidant genes like SOD, GPX, and Peroxiredoxin 6 were significantly upregulated in the TBE plus lutein group.

Lens immunohistochemistry showed reduced NOX-1, 4-HNE, and CEL in the TBE plus lutein group.

Abstract

Trapa bispinosa Roxb. extract (TBE), combined with lutein, has an inhibitory effect on cataract progression. However, no prior studies evaluated oxidative stress- and antioxidant-related factors simultaneously. This study aimed to investigate TBE plus lutein’s potential mechanism to suppress cataract progression and examine its effects on retinal tissue and aorta in spontaneous diabetic Torii (SDT) rats.

Seven-week-old SDT rats (n = 10) and Sprague-Dawley (SD) control rats (n = 5) were divided into three groups: SDT-administered TBE plus lutein (TBE plus lutein), untreated SDT, and control. Blood glucose levels and anterior segment photographs were obtained. Subsequently, polymerase chain reaction (PCR) was used to measure the expression of oxidative stress- and antioxidant-related genes in the lenses, retinas, and aortas. Immunohistochemical staining of the lenses was performed to detect the expression of NOX-1 (an oxidative stress-related factor), 4-HNE (a lipid peroxidation product), and CEL (an advanced glycation end product [AGE]).

The progression of diabetic cataract was suppressed in the TBE plus lutein group. PCR results revealed that NOX-1 in lenses was significantly suppressed in the TBE plus lutein group (p < 0.05), whereas antioxidant-related factors, such as SOD, GPX, and Peroxiredoxin 6, were significantly increased (p < 0.01). A similar trend in NOX-1 expression was observed in the retinas and aortas, but the difference was not significant. Immunohistochemical staining of lenses revealed reduced NOX-1, 4-HNE, and CEL expression in the lenses of the TBE plus lutein group.

TBE plus lutein may inhibit the progression of diabetic cataract by increasing antioxidant-related factors rather than suppressing oxidative stress-related factors.

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