Effect and related mechanism of seaweed polysaccharide on apoptosis of fibroblast-like synoviocytes in patients with rheumatoid arthritis / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the effect and related mechanism of seaweed polysaccharide (SP) on apoptosis of fibroblast-like synoviocytes in patients with rheumatoid arthritis (RA-FLS).</p><p><b>METHODS</b>RA-FLS were in vitro cultured using modified tissue culture method. Effect of SP (0, 15, 20, and 25 mg/mL, respectively) at different time points (0, 3, 4, and 5 days, respectively) on the proliferation and apoptosis of RA-FLS, and protein expressions of Caspase-3, Bax, and Bcl-2 was detected by cell counting kit-8 (CCK-8) assay, Hoechst 33258 staining assay, TUNEL assay, and Western blot, respectively.</p><p><b>RESULTS</b>Compared with 0 mg/mL SP at the same time point, the proliferation of RA-FLS was inhibited, and the apoptosis was promoted 3, 4, and 5 days after intervened by 15, 20, and 25 mg/mL SP, respectively (P<0.01) in time- and dose-dependent manners. RA-FLS Bax protein expression was up-regulated, Bcl-2 protein expression down-regulated, Caspase-3 activated and split by 15, 20, and 25 mg/mL SP, respectively for 4 days (P<0.05, P<0.01). Besides, the changes were in a dose-dependent manner.</p><p><b>CONCLUSIONS</b>SP could inhibit RA-FLS proliferation and induce its apoptosis in dose- and time-dependent manners. Its apoptosis mechanism might be through up-regulating intracellular Bax protein expression and down-regulating Bcl-2 protein expression, thus influencing the mitochondrion signaling pathway, further promoting Caspase-3 activation and split, resulting in the apoptosis of RA-FLS.</p>

Expression of TNF-alpha signaling adapter proteins in peripheral blood mononuclear cells in lupus nephritis patients of different TCM asthenia syndromes / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate the mRNA expressions of the TNF adapter proteins, including TNF receptor-associated death domain protein (TRADD), Fas-associated death domain protein (FADD), receptor-interacting protein 1 (RIP-1) and TNF receptor-associated factor-2 (TRAF-2) in peripheral blood mononuclear cells (PBMCs) of lupus nephritis (LN) patients of various TCM asthenia syndromes. Methods Fifty-one inpatients with LN were differentiated according to TCM syndrome differentiation, 13 cases of yin-deficiency with inner heat syndrome (A); 26 cases of both qi-yin deficiency syndrome (B), 12 cases of Pi-Shen yang-deficiency syndrome (C). Peripheral venous blood samples from the 51 LN patients and 17 healthy subjects were collected to separate PBMCs. The mRNA expressions of TNF adapter molecules (TRADD, FADD, RIP-1 and TRAF-2), as well as Caspase-3 and interleukin-1beta (IL-1beta) were analyzed by quantitative real-time PCR and the differences among them were compared.</p><p><b>RESULTS</b>(1) As compared with the healthy subjects, expression of TRADD mRNA in patients of syndrome A, B and C was lowered to 0.54, 0.32, and 0.38-fold, respectively (P < 0.05, P < 0.01), showing insignificant difference among the three syndromes; (2) FADD mRNA lowered to 0.79, 0.62, and 0.72-fold respectively, only with significance shown in syndrome B (P < 0.05); (3) RIP-1 mRNA lowered to 0.79, 0.50, and 0.60-fold respectively with significance shown in syndrome B and C (P < 0.01, P < 0.05), and insignificant difference was shown among the three syndromes; (4) TRAF-2 lowered to 0.70, 0.52, and 0.50-fold respectively (P < 0.01, P < 0.01, P = 0.07), significance shown in syndrome B and C (P < 0.01), but with insignificant difference among the three; (5) Caspase-3 elevated in all patients of the three syndromes (all P < 0.01); (6) IL-1beta in syndrome A was apparently lower ed to the normal range and also lower than that in the other two syndromes (both P < 0.05).</p><p><b>CONCLUSIONS</b>Expressions of TRADD, FADD, RIP-1 and TRAF-2 mRNA decreased in all the patients of various TCM asthenia syndromes, the decrement in patients of syndrome B and C was lesser than that in syndrome A. These abnormal low expressions of signal proteins might be the substantial bases for asthenia syndromes of LN patients, and the apoptotic signal mediated by them may involve in the formation of asthenia syndrome in LN.</p>