Mechanistically, beyond the intrinsic role of MS’s anti-oxidative, anti-apoptotic and anti-inflammatory effects reported in ischaemia-reperfusion injury models, we found that treatment with MS resulted in a significantly lower level of TNF-α and IL-6 as well as an elevated level of IL-10 upon LPS exposure in macrophages and in animal models. The gene discussed is TNF; the disease is myeloid sarcoma.