To explore the therapeutic capacity of the Liangxue Xiaoban (LXXB) decoction and its disassembled prescriptions in the modulation of T cell subsets and recurrence-related indexes of psoriasis using a psoriasis-like mouse model.

The psoriasis model was generated by the treatment of BALB/c mice (n = 48) with imiquimod. Mice were divided into six groups: control, psoriasis model, tripterygium glycosides, LXXB decoction, Liangxue decoction, and Qingqi decoction. After the intervention period, the interleukin (IL)-17A, IL-22, and interferon-γ levels in mice were examined and hematoxylin and eosin staining was conducted to determine pathological changes in the skin tissues. T cell subset changes in the skin-draining lymph nodes were analyzed using flow cytometry, and the expression levels of the associated transcription factors and recurrence-related indexes in the skin tissues were determined using a polymerase chain reaction.

LXXB decoction attenuated the levels of CD8⁺ T, Th17, and Th1 cells and induced an increase in the Th2 and Treg cell levels. The disassembled prescriptions promoted or inhibited specific subsets of T cells to improve the symptoms of psoriasis. Notably, the LXXB and Liangxue decoctions suppressed the expression of IL-22 at both the gene and protein levels and restored the CD103 and IL-15 expressions in the skin tissue to the normal range.

LXXB decoction exerted significant immunoregulatory effects on T cell subsets and improved the recurrence-related indexes. Interestingly, the Liangxue prescription appeared to have a therapeutic advantage in terms of Th17 modulation and psoriasis recurrence, while the Qingqi prescription performed better in Treg immunoregulation.

The Qinzhi Zhudan formula (QZZD) exhibits a prominent therapeutic effect in the treatment of vascular dementia (VaD). This study combined a network pharmacology approach and experimental validation to identify the underlying biological mechanism of QZZD against VaD.

Male Wistar rats received bilateral common carotid artery occlusion (BCCAO) surgery, and after 4 weeks of intragastric administration of QZZD, the therapeutic effect was assessed using the Morris water maze test and cerebral blood flow (CBF) assessment. Hematoxylin and eosin staining, Nissl staining, and electron microscopy were used to measure the histopathological changes in the neurons of rats. The effect of QZZD treatment on hippocampal neurotransmitters was assessed by high-performance liquid chromatography with electrochemical detection and liquid chromatography mass spectrometry. Immunofluorescence was used to observe VaD-induced microglia activation. The inflammatory cytokine levels were assessed by enzyme linked immunosorbent assay. Western blot was used to examine the TNFR1-mediated TNF pathway, which was screened out by network pharmacology analysis.

QZZD treatment alleviated pathological changes and neuronal damage in VaD rats and attenuated their cognitive impairment. In addition, QZZD increased CBF and the expression of acetylcholine and 5-hydroxytryptamine in the hippocampal region. Notably, QZZD inhibited microglial activation and the expression of IL-6 and TNF-α. Network pharmacology and western blot indicated that QZZD inhibited the levels of TNFR1, NF-κBp65, p-ERK, TNF-α, and IL-6, which are related to the TNFR1-mediated TNF signaling pathway.

QZZD clearly improved learning and memory function, reduced brain pathological damage, elevated CBF and hippocampal neurotransmitter levels, and alleviated neuroinflammation of VaD rats partly by inhibiting the TNFR1-mediated TNF pathway, indicating its potential value in the clinical therapy of VaD.

Inflammation is an essential component of liver diseases. Paeoniflorin (PF), a monoterpenoid component derived from peony root (Paeonia lactiflora Pall.), has anti-inflammatory, immunoregulatory, and hepatoprotective activities. However, whether PF affects liver inflammation and its underlying mechanisms is unclear. In this study, we investigated the effects of PF on lipopolysaccharide (LPS)-induced inflammation in LO2 cells and the underlying molecular mechanism.

LPS was used to induce inflammation. After PF pretreatment for 2 h, the cells were treated with PF and LPS. Cell counting kit-8 was used to measure cell viability. Tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 were tested by Enzyme-linked immunosorbent assay. Western blot was used to evaluate TNF-α, Ras homolog family member A (RhoA), NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, and IL-1β proteins expression.

In LPS-induced LO2 cells, PF reduced TNF-α and IL-6 inflammatory cytokine production in a dose-dependent manner. LPS-induced TNF-α expression was also suppressed by PF. In addition, PF significantly inhibited LPS-induced RhoA activation (P = .0014). Finally, PF suppressed LPS-induced NLRP3 inflammasome activation by downregulating NLRP3, ASC, caspase-1, and IL-1β expression.

These findings suggest that PF alleviates inflammation induced by LPS and further suggest the anti-inflammatory effect of PF may follow via reduced RhoA and NLRP3 inflammasome activity.