Objective To observe the effects of recombinant human endostatin(rhEndostatin) on intracellular CaSUP>2+/SUP> homeostasis in fibroblastlike synoviocytes(FLSs) in rats with adjuvant arthritis(AA), approach ionic mechanisms of AA FLSs apoptosis induced by rhEndostatin, and provide experimental data for possible drug treatment and their targets in rheumatoid arthritis (RA). Methods Twelve male SpragueDawley(SD) rats weighing 140160 g were used for these studies. The rats were divided at random into a normal group (EM>n/EM>=3) and an AA model group (EM>n/EM>=9). Adjuvant arthritis was induced in rats in the AA model group and the FLSs obtained from AA rats were cultured EM>in vitro/EM>. The cultured AA FLSs were incubated with the calcium ionsensitive fluorescent indicator fluo3/AM. A confocal laser scanning microscope was used to measure changes of fluorescence intensity of intracellular CaSUP>2+/SUP> in the cells caused by rhEndostatin when the cells were immersed in buffer (with or without CaSUP>2+/SUP>), and to investigate the effect of rhEndostatin on intracellular free calcium concentration {［CaSUP>2+/SUP>］i} in AA FLS. Results Recombinant human endostatin could cause rapid ［CaSUP>2+/SUP>i elevation in static AA FLSs in CaSUP>2+/SUP>containing buffer. Within 10s after treatment with rhEndostatin, the elevated levels of ［CaSUP>2+/SUP>］i ran rapidly to peaked and was followed by a plateau period. The elevated ［CaSUP>2+/S