包装 | 价格(元) |
5mg | 电议 |
10mg | 电议 |
25mg | 电议 |
50mg | 电议 |
Cell experiment: | To choose a sublethal concentration of N-Acetylcysteine amide and N-acetylcysteine for the study on their ability to protect cells from doxorubicin (DOX)-induced toxicity, H9c2 cells are exposed with N-Acetylcysteine amide or N-acetylcysteine at 0.25 mM, 0.50 mM, 0.75 mM, 1 mM, 2 mM, 5 mM, 10 mM, and 20 mM for 24 h. Untreated cells are used as the control for each experiment[1]. |
Animal experiment: | Rats[2]In order to assess mitochondrial respiration and glutathione content following traumatic brain injury (TBI), rats are randomly divided into three groups (n = 5 animals/group). (I.) N-Acetylcysteine amide group receives multiple bolus IP injections of N-Acetylcysteine amide (150 mg/kg) immediately after 5 minutes and then every 6 hours up to 24 hrs post-injury. (II.) Vehicle group receives equivalent v/v saline at 5 minutes and every 6 hours (6, 12, 18, 24 hrs) up to 24 hrs post-injury. (III.) Sham injured group animals do not receive any drug treatment. At 25 hrs post-injury, all animals are euthanized and mitochondria are isolated from the ipsilateral cortical hemisphere (6 mm punch) to carry out measurements of mitochondrial respiration and glutathione content[2]. |
产品描述 | N-Acetylcysteine amide is a cell membranes and blood brain barrier permeant thiol antioxidant and neuroprotective agent, reduces ROS production. N-Acetylcysteine amide shows no obvious effect on the viability of H9c2 cells treated with doxorubicin (DOX) at< 1 mM, but causes significant cytotoxicity at 10-20 mM. N-Acetylcysteine amide (750 μM) reduces the ROS levle and lipid peroxidation induced by DOX, and restores GSH/GSSG ratio and activities of antioxidant enzymes, such as catalase (CAT), gluthathione peroxidase (GPx), gluthathione reductase (GR)[1]. N-Acetylcysteine amide (1 mM) protects the human brain microvascular endothelial (HBMVEC) from methamphetamine (METH)- induced cell death[3]. N-Acetylcysteine amide has increased CNS bioavailability. N-Acetylcysteine amide (150 mg/kg, i.p.) improves cortical sparing and functional outcome, reduces oxidative stress, improves mitochondrial bioenergetics, and maintains mitochondrial glutathione content following traumatic brain injury (TBI) in rats[2]. References: |