ArticleMolecular neurobiology2025
Sagittaria Sagittifolia Polysaccharide Ameliorates Diabetic Retinopathy in Mice via Inhibiting TLR4-Mediated Microglial Activation.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Exogenous Hormones Affect the Corm Expansion ofPlants (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Sagittaria sagittifolia polysaccharide (SSP) exhibits anti-inflammatory, antioxidant, lipid-regulating, and hypoglycemic properties, demonstrating therapeutic potential against diabetic retinopathy (DR). This study aimed to investigate the intervention efficacy of SSP in DR mice and its regulatory effects on retinal microglia activation. The type 2 diabetic mouse model was established by high-fat diet feeding combined with streptozotocin (STZ) intravenous injection. At week 9, retinal vascular pathology was assessed via fundus photography and fluorescein angiography. Serum lipid metabolism TG, CHO, LDL, and HDL were quantified using an automated biochemical analyzer. Retinal histopathology and thickness were evaluated through HE staining combined with Evans blue staining. Microglial activation adjacent to retinal vasculature was visualized by immunofluorescence, while retinal apoptosis was examined using immunohistochemistry and TUNEL staining. Co-localization of TLR4 and Iba was analyzed by immunofluorescence. Protein expression levels of TLR4, Myd88, P-p65, and total p65 in retinal tissues were determined by Western blot. SSP treatment significantly attenuated DR progression, as evidenced by preserved retinal vascular integrity, restored retinal thickness, reduced vascular leakage, lowered fasting blood glucose, and regulated lipid metabolism (reduced TG/TC/LDL-C, increased HDL-C). Furthermore, SSP suppressed pathological recruitment of microglia to retinal vasculature and inhibited their pro-inflammatory morphological transition. Mechanistically, SSP downregulated TLR4/Iba co-expression and inhibited the downstream Myd88/NF-κB signaling pathway. The study results demonstrated that SSP can delay the progression of retinopathy in type 2 diabetic mice. This mechanism seems to be associated with SSP's hypoglycemic and lipid-regulating effects, along with its inhibition of microglia-mediated inflammatory responses.
Indexed as
Identifiers
41288786What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.