ArticleMolecular neurobiology2026
Fuzheng Jiedu Tongluo Granule Alleviates Cerebral Ischemia/reperfusion Injury-induced Inflammation By Inhibiting Drp1-mediated TXNIP/NLRP3 Pathway.
Article in Molecular neurobiology, 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
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory response is considered a critical component in developing cerebral ischemia/reperfusion injury (CI/RI). Dynamin-related protein 1 (Drp1) performs an essential role in initiating and advancing CI/RI-induced inflammatory reactions. The objective of the present study was to investigate whether Fuzheng Jiedu Tongluo Granule (FZJDTL) attenuated CI/RI by modulating the Drp1-mediated TXNIP/NLRP3 pathway in vivo and in vitro. Molecular docking and molecular dynamics simulations validated the interactions between the core target and the main components of FZJDTL. Oxygen-glucose deprivation/reoxygenation (OGD/R) in PC12 cells and middle cerebral artery occlusion/reperfusion (MCAO/R) in rats were established. Then, the neuroprotective effects of FZJDTL in MCAO/R rats were assessed using brain infarct volume, HE staining, and neurological deficit scores. The levels of inflammatory factors were detected by ELISA. We further examined whether the neuroprotective effect of FZJDTL on MCAO/R in rats and OGD/R in PC12 cells was connected to the suppression of the Drp1-mediated TXNIP/NLRP3 pathway through methods of Western blot and RT-qPCR. Molecular docking and molecular dynamics simulations revealed that the principal components of FZJDTL exhibited favorable binding affinity with Drp1. The results demonstrated that FZJDTL mitigated pathological brain damage, ameliorated neurological impairments, and reduced the volume of cerebral infarction. FZJDTL inhibited the production of ROS and inflammatory factors (IL-1β, IL-18). In vivo and in vitro studies revealed that the neuroprotective effect of FZJDTL was associated with Drp1-mediated modulation of the inflammatory response, as evidenced by the suppression of mRNA and protein expression of p-Drp1, TXNIP, NLRP3, GSDMD, GSDMD-N, Caspase-1, Cleaved caspase-1, and ASC. Besides, FZJDTL significantly upregulated the mRNA and protein expression of OPA1 and TRX, as verified by RT-qPCR and Western blot analysis. Taken together, treatment with FZJDTL attenuated CI/RI by reducing the inflammatory response via the Drp1-mediated TXNIP/NLRP3 pathway.
Indexed as
Identifiers
42113382What 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.