| 包装 | 价格(元) |
| 5g | 电议 |
| 10g | 电议 |
| 25g | 电议 |
Cell lines | LNCaP cells |
Preparation Method | Real-time PCR amplification of the total DNA from M. hyorhinis -infected LNCaP cells cultured for 48 h in the presence of varying concentrations of Hemin chloride. |
Reaction Conditions | 100 µM Hemin chloride for 48 h |
Applications | Hemin chloride treatment induces HO-1 expression and inhibits M. hyorhinis replication in LNCaP prostate cancer cells. |
Animal models | C57BL/6 mice |
Preparation Method | House dust mite (HDM)-sensitized and challenged mice were instilled intranasally with 100 µg Hemin chloride-DCEVs at 1 d before sensitization and challenge. |
Dosage form | 100 µg Hemin chloride-DCEVs at 1day |
Applications | In HDM-induced asthmatic mouse model, Hemin chloride-DCEVs inhalation reduced eosinophils infiltration and mucus secretion in the airway, decreased the levels of IL-4, IL-5, and IL-13 in the lung and the number of Th2 cells in mediastinal lymph nodes (MLNs), and increased the number of Treg cells in MLNs. |
| 产品描述 | Hemin chloride, a substrate of heme oxygenase (HO)-1, induces HO-1 expression on a variety of cells to exert anti-oxidant and anti-inflammatory roles. A dramatic reduction of cell-associated M. hyorhinis DNA in a dose-dependent manner, with > 90% inhibition at 100 μm Hemin chloride. Hemin chloride treatment profoundly inhibited intracellular M. hyorhinis DNA levels within 10 h to nearly undetectable levels after 48 h[1]. Macrophage exposed to Hemin chloride exhibits modulation of non-opsonic phagocytosis of aged RBCs, ability to kill bacteria and secretion of cytokines.Translocation and sequestration of CD36 within the intracellular storage in the Hemin chloride treated macrophages. It in-turn modulates the global cytokine secretion from macrophages. CD36 has strong affinity for Hemin chloride with a dissociation constant of 1.26 ±0.24 μM[3]. Hemin chloride treatment decreased cell proliferation to 62.5 %, 51.3 %, and 38.8 % in PA-TU-8902, BxPC-3 and MiaPaCa-2 cancer cells, respectively. Enhancement of anti-proliferative effects of statins by Hemin chloride, documented as decreased cell proliferation after 48 h of co-treatment[5]. The presence of Hemin chloride in irradiated lung cancer cells enhanced the productivity of initial ROS, resulting in lipid peroxidation and subsequent ferroptosis[6]. In HDM-induced asthmatic mouse model, Hemin chloride-DCEVs inhalation reduced eosinophils infiltration and mucus secretion in the airway, decreased the levels of IL-4, IL-5, and IL-13 in the lung and the number of Th2 cells in mediastinal lymph nodes (MLNs), and increased the number of Treg cells in MLNs[2]. Hemin chloride-preconditioned mice exhibited preserved renal cell function, and the tubular injury score at 72h indicated that tubular damage was prevented[4]. When compared with wild-type littermates, the mortality for SS Cttn+/- mice trended to be lower after Hemin chloride infusion and these mice exhibited less severe lung injury and less necroptotic cell death[7]. References: |
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