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Mechanistic study of compound Muniziqi granule on lupus nephritis in MRL/lpr mice: insights from transcriptomics and
Jiyun Zhang1, Yuming Wang2, Cuiting Gong3
1The Second Affiliated Hospital of Xinjiang Medical University, Urumqi Municipality, Xinjiang, China.
Background:
Lupus 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.
Methods:
CMG 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.
Results:
CMG 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.
Conclusion:
CMG 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.
