Objective: To observe the therapeutic efficacy of combined therapy with ginsenosides (GS) and prednisone on systemic lupus erythematosus (SLE).

Methods: Sixty patients with SLE were assigned to 2 groups randomly by a randomizing digital table, the treated group and the control group, 30 cases in each group. All patients were treated with routine administration of prednisone, but to the treated group GS Capsule (50 mg) was given additionally twice every day, while to the control group placebo capsule of equal dosage was given instead. The total clinical efficacy, and changes of systemic lupus erythematosus disease activity index (SLEDAI), erythrocyte sedimentation rate (ESR), complement 3 (C3) and anti-ds-DNA were observed after 3-month-treatment.

Results: The total clinical efficacy rate was 89.28% in the treated group and 66.67% in the control group, showing a significant difference between them (P<0.05). The improvements of SLEDAI, ESR and C3 in the treated group were more significant than those in the control group (P<0.01, P<0.05).

Conclusion: The combined therapy of GS and prednisone could enhance the clinical efficacy, reduce the SLEDAI and promote the recovery of laboratory indices in SLE patients.

Download full-text PDF

Source

Publication Analysis

Top Keywords

systemic lupus
12
treated group
12
control group
12
combined therapy
8
therapy ginsenosides
8
ginsenosides prednisone
8
lupus erythematosus
8
total clinical
8
clinical efficacy
8
group
7

Similar Publications

Essential Thrombocythemia: A Review.

JAMA

January 2025

CRIMM, Center Research and Innovation of Myeloproliferative Neoplasms, University of Florence, AOU Careggi, Florence, Italy.

Importance: Essential thrombocythemia, a clonal myeloproliferative neoplasm with excessive platelet production, is associated with an increased risk of thrombosis and bleeding. The annual incidence rate of essential thrombocythemia in the US is 1.5/100 000 persons.

View Article and Find Full Text PDF

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the production of autoantibodies and damage to multiple organs. Glomerulonephritis, a manifestation involving glomerular deposition of immune complexes and complement components, significantly contributes to disease morbidity. Although the endosomal single-stranded RNA sensor TLR7 is known to drive glomerulonephritis by promoting autoantibody production in B cells, the contribution of macrophage TLR7 responses to glomerulonephritis remains poorly understood.

View Article and Find Full Text PDF

This 30-color panel was developed to enable the enumeration and purification of distinct circulating immune cell subsets implicated in the pathogenesis of systemic autoimmune diseases including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc; scleroderma), Sjögren's disease (SjD), idiopathic inflammatory myopathy (IIM), and others. While designed for application to peripheral blood mononuclear cells, the inclusion of CD45 coupled with the ability to extract cellular autofluorescence spectral signatures enables the application of this panel to other tissue types. Of the 30 total markers, this panel employs 18 markers to profile T cell subsets consisting of different memory subsets and T helper polarities, > 10 markers to profile B cell subsets including double-negative B cells, and a total of 8 lineage markers to identify immune lineages including monocyte and natural killer cell subsets, conventional dendritic cells, plasmacytoid dendritic cells, and basophils.

View Article and Find Full Text PDF

LAIR1 is an inhibitory receptor broadly expressed on human immune cells, including B cells. LAIR1 has been shown to modulate BCR signaling, however, it is still unclear whether its suppressive activity can be a negative regulator for autoreactivity. In this study, we demonstrate the LAIR1 expression profile on human B cells and prove its regulatory function and relationships to B cell autoreactivity.

View Article and Find Full Text PDF

While durable antibody responses from long-lived plasma cell (LLPC) populations are important for protection against pathogens, LLPC may be harmful if they produce antibodies against self-proteins or self-nuclear antigens as occurs in autoimmune diseases such as systemic lupus erythematosus (SLE). Thus, the elimination of autoreactive LLPC may improve the treatment of antibody-driven autoimmune diseases. However, LLPC remain a challenging therapeutic target.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!