ArticleArchives of medical science : AMS2013
The effect of esculentoside A on lupus nephritis-prone BXSB mice.
Article in Archives of medical science : AMS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- Studies Related to the Involvement of EsA in Improving Intestinal Inflammation in Acute Pancreatitis via the NF-Mediators of inflammation · 2024Article
- Esculentoside A could attenuate apoptosis and inflammation in TNBS-induced ulcerative colitis via inhibiting the nuclear translocation of NF-κB.Annals of translational medicine · 2022Article
- Comparison of immunohistochemistry and mRNAOncology letters · 2015Article
- Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEsA was reported to have the effect of modulating immune response, cell proliferation and apoptosis as well as anti-inflammatory effects in acute and chronic experimental models. However, the effects of EsA on LN remain poorly understood. To investigate the roles of EsA in LN, the effects of EsA were tested on BXSB mice, a SLE model, in which male SB/Le mice and female C57BL/6 mice were hybridized through recombinant inbred species. MATERIAL AND
methodsTwenty four BXSB mice were divided into three groups. After 4 weeks, blood samples, urine samples and kidney tissues were collected. Measurement of cytokine levels was carried out using sandwich ELISA reagent kits. Apoptotic scores were obtained with a TUNEL assay. PCNA and Caspase-3 mRNA was detected using the In Situ Hybridization Detection Kit.
resultsThe results demonstrated that compared with the control group, EsA administration markedly controlled urine protein excretion, improved renal function, alleviated kidney damage and promoted the apoptosis of glomerular intrinsic cells and renal tubular epithelial cells in animals of the treated group (p < 0.05). Meanwhile, EsA reduced the serum IL-6 and TNF-α levels (p < 0.05), inhibited the expression of PCNA and promoted the expression of caspase-3, Fas and FasL in animals of the treated group (p < 0.05). The effects of EsA on BXSB mice were similar to dexamethasone.
conclusionsAll these findings indicated that EsA might play significant roles in the treatment of BXSB mice through modulation of inflammatory cytokines, inhibition of renal cell proliferation and induction of apoptosis. The special targets of EsA in lupus nephritis are worth further exploration.
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