Surface-enhanced Raman scattering (SERS) is a very important tool in vibrational spectroscopy.

Background: Lupus nephritis (LN) is a serious complication of systemic lupus erythematosus (SLE) and is difficult to cure. Lang Chuang Wan (LCW) has been widely used in clinical practice as a treatment for SLE and LN, but its active ingredients and mechanism of action have not been elucidated. To address this, we aim to analyze LCW’s chemical components and clarify its mechanisms in treating LN. Methods: We utilized ultra-performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS) to analyze the components of LCW and assessed its effects on MRL/lpr mice through ELISA, H&E staining, Masson’s trichrome staining, and IgG immunofluorescence. Then, we further explored the mechanisms of action through network pharmacology, transcriptomics, and metabolomics, and validated with Western blot. Results: LCW contained 1303 chemical components, primarily flavonoids and terpenoids. It significantly improved kidney pathology and normalized levels of serum ANA, anti-dsDNA, anti-Sm, C3, C4, Cr, BUN, IL-6, IL-10, IL-17, TNF-α, and urinary protein (UP) in MRL/lpr mice. Network pharmacology, transcriptomics, and metabolomics indicated that LCW’s therapeutic effect on LN involved the PI3K/AKT pathway, confirmed by Western blot showing LCW’s suppression of the PI3K/AKT/mTOR pathway. Conclusions: LCW alleviates pathological symptoms in MRL/lpr mice by inhibiting the PI3K/AKT/mTOR signaling pathway, providing insights into its therapeutic mechanisms for lupus nephritis.

Background: Alzheimer’s disease (AD), a progressive brain disorder, is the most common form of dementia and necessitates the development of effective intervention strategies. Ginseng-Natto composite fermentation products (GN) have demonstrated beneficial bioactivities in mouse models of AD; however, the underlying mechanism of action through which GN ameliorates AD requires further elucidation. Methods: Mice received daily intragastric administration of low- or high-dose GN for 4 weeks, followed by intraperitoneal injection of scopolamine to induce the AD model. The pharmacological effects of GN were systematically evaluated using the Morris water maze test, ELISA, and H&E staining. To further investigate the underlying mechanisms, 16S rRNA gene sequencing and metabolomics were employed to analyze the regulatory effects of GN on the gut–brain axis. Additionally, Western blotting was performed to assess the impact of GN on blood–brain barrier (BBB) integrity. Results: GN intervention significantly ameliorated cognitive deficits and attenuated neuropathological injury in AD mice, restoring the brain levels of acetylcholine (ACh), acetylcholinesterase (AChE), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) to normal ranges. GN reshaped the gut microbiota by promoting beneficial bacteria and inhibiting pro-inflammatory strains. It also regulated key metabolic pathways related to amino acid and unsaturated fatty acid metabolism. This metabolic remodeling restored the compromised BBB integrity by upregulating tight junction proteins (ZO-1, Occludin and Claudin-1). Conclusions: Our findings demonstrate that GN ameliorates AD through a gut-to-brain pathway, mediated by reshaping the microbiota-metabolite axis and repairing the BBB. Thus, GN may represent a promising intervention candidate for AD.

Background: Lupus nephritis (LN), a severe complication of systemic lupus erythematosus (SLE), necessitates effective therapeutic strategies. Polysaccharides derived from Irpex lacteus have demonstrated beneficial biological activities in MRL/lpr mice; however, their precise mechanisms of intervention in LN require further elucidation. Methods: MRL/lpr mice were administered low-dose and high-dose Irpex lacteus polysaccharide (PCP) continuously for 8 weeks. The therapeutic efficacy of PCP was systematically assessed by measuring autoantibody levels, inflammatory cytokine expression, and renal function markers. The underlying pharmacological mechanisms were investigated through integrated transcriptomics and metabolomics analyses. Results: PCP treatment significantly improved renal function in MRL/lpr mice, normalizing serum levels of anti-nuclear antibodies (ANA), anti-double-stranded DNA antibodies (anti-dsDNA), anti-Sm antibody (Sm), creatinine (Cr), blood urea nitrogen (BUN), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and proteinuria. Integrated transcriptomic and metabolomic analyses revealed that the therapeutic action of PCP involves modulation of the PI3K/AKT/NF-κB pathway. This inhibition was further confirmed by Western blot analysis. Conclusions: PCP exerts renal protective effects in MRL/lpr mice by mitigating inflammation, modulating immune responses, and preserving renal function. The combined application of transcriptomics, metabolomics, and Western blotting elucidates that this protection is mediated through inhibition of the PI3K/AKT/NF-κB signaling pathway.