| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
Cell lines | human pulmonary microvascular endothelial cells |
Preparation Method | In the hydrogen peroxide (H2O2)-induced oxidative stress in lung cell assay, cells were exposed to 100 μM H2O2with WKYMVm treatment. After incubation with WKYMVm for 24 hours in 96-well plates, the cell counting kit (CCK)-8 assay was carried out to determine the relative cell proliferation rate (%), according to the manufacturer’s instructions. |
Reaction Conditions | 100 μM, 24 h |
Applications | In human pulmonary microvascular endothelial cells (HULEC-5a) and primary murine pulmonary endothelial and epithelial cells, 1 and 100 μM WKYMVm treatments significantly increased proliferation in both the control and H2O2-exposed groups. |
Animal models | male C57/BL6J mice |
Preparation Method | A total of 20 male C57/BL6 mice, eight‐week‐old, were split randomly into four equal groups: sham, LPS, low‐dose WKYMVm (4 mg/kg bodyweight) and high‐dose WKYMVm (8 mg/kg bodyweight). The sham and LPS group were injected with PBS and LPS (5 mg/kg bodyweight), respectively. Predetermined WKYMVm doses were mixed with LPS and injected into the mice in combination. Injections were performed subcutaneously against the skull altogether 7 times with 48 hours intervals between applications. |
Dosage form | 4 mg/kg and 8 mg/kg;s.c. |
Applications | WKYMVm protected against LPS‐induced bone loss in vivo. |
| 产品描述 | WKYMVm is a potent N-formyl peptide receptor (FPR1) and FPRL1/2 agonist, and also activate phosphoinositide hydrolysis in undifferentiated HL-60 cells.[1] In vitro efficacy test indicated that treatment with 0.01, 0.1, 1 and 10 μmol/L WKYMVm for 24 hours or 48 hours obviouly suppressed RANKL‐induced mature osteoclasts.[3]In vitro, treatment with 10 μM WKYMVm to stimulate FPR2 can induce p47phox phosphorylation in IMR90 fibroblasts and in human lung cancer cells, which is considered the key event for NADPH oxidase-dependent superoxide generation. Moreover, 10 μM WKYMVm to stimulate also induced NADPH oxidase-dependent superoxide generation with maximal production occurring at 2 min.[6] In vivo experiment it shown that treatment with 2.5- and 5 mg/kg/d daily over four days intraperitoneally in ALI mice decreased the levels of proinflammatory cytokines TNF-α, IL-6, and IL-1β, while it increased the MPO and NO release by differentiated HL-60 neutrophil-like cells.[2]. Intramuscular injection of 10–5 mol/l WKYMVm improves blood perfusion and provides protection from tissue damage in the ischemic hind limb.[4]In vivo, treatment with 8 mg/kg WKYMVm subcutaneously (at 0, 12, 24, 36, 48 and 60 h) effectively attenuated the DSS-induced increase in the bleeding score and the stool score and protects dextran sodium sulfate (DSS)-induced experimental ulcerative colitis.[5]In addition, administration of 4 mg/kg WKYMVm, to septic mice strongly increased neutrophil number through augmented emergency granulopoiesis[7]. References: |
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