30 results about "L929 cell" patented technology

Provided is high-strength high-plasticity biodegradable Zn-Mn-Li zinc alloy. The alloy comprises 0.01-0.8% of Mn and 0.005-0.4% of Li, wherein Mn is the main alloying element, Li is the minor alloyingelement, and the content of Mn is not lower than the content of Li in the alloy; at least one of Na, K, Ca, Sr, Ti, Mg, Fe, Cu and Ag is selected, wherein the content of Na and the content of K are both not higher than 0.1%, and the total content of Na, K and Li is not higher than 0.4%; the content of Ca, the content of Sr, the content of Ti and the content of Mg are all not higher than 0.2%, andthe total content of Ca, Sr, Ti and Mg is not higher than 0.2%; the content of Fe is not higher than 0.05%; the adding amount of Cu and the adding amount of Ag are not higher than 0.4%, and the totalcontent of Cu and Ag is not higher than 0.4%; and the total content of alloy elements added into the Zn-Mn-Li zinc alloy is not higher than 1.8%, and the balance Zn. The yield strength of the zinc alloy is 250-450 MPa, the tensile strength of the zinc alloy is 350-600 MPa, and the ductility is 20-60%; the degrading rate in simulated body fluid is not higher than 0.15 mm / year; the cytotoxicity tothe L929 cell is at the level 0 or level 1, and good cytocompatibility is presented. The zinc alloy is used for a degradable bracket or other medical implants.

The present invention relates to an isoxazole derivative, the compound of formula (I)herein after referred to as GIT27-NO, which is the NO-donating structurally modified form of (S,R)-3-phenyl-4,5-dihydro-5-isoxazole acetic acid, herein after referred to as VGX-1027. Treatment of three tumor cell lines, rat astrocytoma C6, mouse fibrosarcoma L929, and mouse melanoma B16 cells with GIT27-NO resulted in a significant reduction of cell respiration and of number of viable cells, while VGX-1027 was completely ineffective. Hemoglobin, which act as NO-scavenger, restored cell viability, thus indicating the NO-mediated tumoricidal effect of compound (I). GIT27-NO triggered apoptotic cell death in L929 cell cultures, while autophagic cell death is mainly responsible for the diminished viability of C6 and B16 cells. Moreover, GIT27-NO induced the production of reactive oxygen species which can be neutralized by antioxidant N-acetyl cysteine (NAC), indicating that reactive oxygen species (ROS) are at least partly involved in the reduction of cell viability. The anti-tumor activity of GIT27-NO is mediated through activation of MAP kinases (ERK1 / 2, p38 and JNK) in cell-specific manner. The role of MAP kinases was further confirmed by specific inhibitors of these molecules, PD98059, SB202190, and SP600125. Finally, in vivo treatment with GIT27-NO significantly reduced tumor growth in syngeneic C57BL / 6 mice implanted with B16 melanoma.