Experimental research
The effect of esculentoside A on lupus nephritis-prone BXSB mice
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Submission date: 2011-11-15
Final revision date: 2012-02-27
Acceptance date: 2012-02-29
Online publication date: 2012-10-30
Publication date: 2013-04-30
Arch Med Sci 2013;9(2):354–360
Introduction: Esculentoside A (EsA), a saponin isolated from the root of Phytolacca esculenta, 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 lupus nephritis (LN) remain poorly understood. To investigate the roles of EsA in LN, the effects of EsA were tested on BXSB mice, a systemic lupus erythematosus (SLE) model, in which male SB/Le mice and female C57BL/6 mice were hybridized through recombinant inbred species.
Material and methods: Twenty 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 terminal transferase-mediated dUTP nick-end labeling (TUNEL) assay. PCNA and Caspase-3 mRNA was detected using the In Situ Hybridization Detection Kit.
Results: The 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. Meanwhile, EsA reduced the serum interleukin-6 (IL-6) and tumour necrosis factor a (TNF-α) level, inhibited the expression of proliferating cell nuclear antigen (PCNA) and promoted the expression of caspase-3, Fas and FasL in animals of the treated group. The effects of EsA on BXSB mice were similar to dexamethasone.
Conclusions: All 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.