ArticleLupus science & medicine2026
Mechanistic study of compound Muniziqi granule on lupus nephritis in MRL/lpr mice: insights from transcriptomics and experimental validation.
Article in Lupus science & medicine, 2026. 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
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLupus nephritis (LN) is a severe and prevalent complication of SLE. Compound Muniziqi granule (CMG), a traditional remedy, is commonly used to treat immune system-related disorders. However, its efficacy in treating LN remains unassessed. This study aims to evaluate the therapeutic potential of CMG for LN and to explore its molecular mechanisms.
methodsCMG was evaluated for therapeutic effects on LN in Murphy Roths Large (MRL)/lymphoproliferation (lpr) mice. Renal tissues from mice in the Control, Model and CMG treatment groups were collected for transcriptomic analysis to identify the potential pathways involved in CMG's action in LN. We then examined the effects of CMG on inflammatory cell infiltration, complement system activation and B-cell accumulation in the renal tissues of MRL/lpr mice. Additionally, we assessed the impact of CMG on the cluster of differentiation 40 (CD40)/Nuclear Factor-kappa B p65 (NF-κB p65) signalling pathway in these tissues.
resultsCMG treatment reduced the spleen index in MRL/lpr mice, decreased serum levels of antibodies and inflammatory cytokines and improved renal function markers. It also alleviated renal pathological damage and inflammatory infiltration. Transcriptomic analysis indicated that CMG's therapeutic effects may be linked to 'SLE' and the 'NF-κB signalling pathway'. Further investigation revealed that CMG downregulated a wide array of complement-related and inflammation-associated genes. Notably, CMG reduced the gene expression of CD40 and CD40L. In addition, CMG decreased inflammatory cytokine levels. Preliminary immunofluorescence analysis indicated that CMG reduced immune complex deposition and diminished B-cell infiltration in the renal tissues of MRL/lpr mice. Preliminary western blot analysis indicated that CMG downregulated B Lymphocyte-Induced Maturation Protein 1 (BLIMP1), CD40 and tumour necrosis factor (TNF) receptor-associated factor 6 (TRAF6) expression, as well as the phosphorylation of NF-κB p65.
conclusionCMG effectively mitigates inflammatory infiltration and renal damage in MRL/lpr mice. Preliminary evidence indicates that this protective effect may be associated with reduced activity of the CD40/NF-κB p65 signalling pathway, along with decreased B-cell activation and complement system activation.
Indexed as
Identifiers
What 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.