Sodium Lauryl Sulfoacetate

Treatment with Sodium Lauryl Sulfoacetate results in an increase in the expression of c-Fos protein in macrophages, while the phosphorylation level of extracellular signal-related kinase 1/2 (ERK1/2) is not affected by the treatment^[2].

The primary cells are equally divided into five groups as follows: the control group (group 1), cells treated with 25 μg/ml Sodium Lauryl Sulfoacetate (group 2), 50 μg/ml Sodium Lauryl Sulfoacetate (group 3), 100 μg/ml Sodium Lauryl Sulfoacetatee (group 4) and 200 μg/ml Sodium Lauryl Sulfoacetate (group 5). Group 1 is administered an equivalent amount of normal saline (NS), whilst groups 2 to 5 are treated with corresponding amounts of Sodium Lauryl Sulfoacetate. NS and Sodium Lauryl Sulfoacetate are administered daily for 7 days by transfer pipette. Following the final administration, the five groups of synovial cells are measured using an MTT assay for analysis of the growth inhibitory rate of SH on synovial proliferation.

Sodium Lauryl Sulfoacetate has been shown to protect against cationized bovine serum albumin (C-BSA)-induced glomerulonephritis in BALB/C mice through the suppression of the urine protein, morphological character and monocyte chemotactic protein 1 (MCP-1). In addition, Sodium Lauryl Sulfoacetate treatment has been shown to induce a respiratory burst and to increase the concentration of free calcium in macrophages, as well as increase IL-2 within T-cells. Sodium Lauryl Sulfoacetate in the serum, stomach and intestine can be detected immediately by GC at 0.5 h. The concentration of Sodium Lauryl Sulfoacetate in the stomach gradually increases from 0.5–2 h, but is drastically reduced at 4 h. Furthermore, the concentration in the serum and intestine at 1–4 h decreases in a time-dependent manner, indicating that Sodium Lauryl Sulfoacetate can be quickly absorbed into the circulatory system and intestine and might be quickly distributed to other organs, such as trachea, lung, brain, heart and kidney^[2].