ArticleIn vitro cellular & developmental biology. Animal2026
Huwang Mingmu decoction protects retinal neurons in early diabetic retinopathy by suppressing the IL-1β-c-Jun-GS pathway: an in vivo and in vitro study.
Article in In vitro cellular & developmental biology. Animal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Huwang Mingmu decoction (HWMMT) is a traditional Chinese herbal formula used clinically for diabetic retinopathy (DR), but its neuroprotective mechanisms remain unclear. This study aimed to investigate whether HWMMT protects retinal neurons in early DR by attenuating glutamate excitotoxicity via the IL-1β/c-Jun/glutamine synthetase (GS) signaling axis. Diabetes was induced in Sprague-Dawley rats by streptozotocin injection, and animals were randomized into control, diabetic model (DM), and HWMMT-treated diabetic (DM + HWMMT) groups. HWMMT was orally administered for 8 wk, with body weight and blood glucose monitored weekly. At weeks 4 and 8, retinal tissues and serum were collected for qRT-PCR, Western blotting, and ELISA. In vitro, primary rat retinal Müller glial cells (Müller) were cultured and assigned to five groups: blank control, HWMMT serum control, high-glucose (HG), HG + HWMMT, and HG + HWMMT + IL-1β (rescue group). Cell viability, LDH release, glutamate secretion, apoptosis, and expression of IL-1β, c-Jun, and GS were evaluated. In vivo, DM rats showed slower weight gain, sustained hyperglycemia, upregulated retinal IL-1β and c-Jun expression, downregulated GS, and elevated serum glutamate; HWMMT treatment significantly reversed these abnormalities. In vitro, HG exposure decreased Müller cell viability, increased apoptosis, LDH leakage and glutamate release, and induced IL-1β/c-Jun upregulation with GS downregulation; co-treatment with HWMMT-containing serum reversed all these changes. Notably, exogenous IL-1β supplementation significantly attenuated the cytoprotective and anti‑apoptotic effects of HWMMT and reversed its modulation of IL-1β, c-Jun, GS, and glutamate homeostasis. Collectively, these findings demonstrate that HWMMT exerts neuroprotection in early DR by suppressing the IL-1β/c-Jun signaling cascade and restoring GS expression and function in Müller cells, thereby reducing extracellular glutamate accumulation and mitigating excitotoxic damage. The rescue experiments further support that HWMMT acts specifically through this pathway, providing mechanistic insight and preclinical evidence for HWMMT as a potential therapeutic intervention for early diabetic retinopathy.
Indexed as
Identifiers
42758256What OpenQuestion 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 OpenQuestion graph.