Anti-BAX monoclonal antibody

MicroRNAs (miRNAs) are reported to be involved in renal hypoxia/reoxygenation (H/R) damage. To investigate this further, human kidney (HK-2) cells were cultured, subjected to H/R and the function of miR-30a-5p and glutamate dehydrogenase 1 (GLUD1) was evaluated. The results showed that, miR-30-5p was downregulated and GLUD1 was upregulated in HK-2 cells exposed to H/R. The relationship between miR-30a-5p and GLUD1 was determined using dual luciferase assays. Primary HK-2 cells were cultured in H/R and transfected with negative control 1 (NC1), negative control 2 (NC2), mimic, inhibitor or GLUD1 siRNA plasmids. Reactive oxygen species (ROS) generation, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and the rate of apoptosis in HK-2 cells were assessed. The results showed that, miR-30a-5p mimic reduced the production of ROS in HK-2 cells treated with H/R, but increased the activity of SOD, CAT and GPx. In addition, miR-30a-5p mimic significantly decreased H/R-mediated apoptosis, decreased the expression of bax and activity of caspase-3 and enhanced the expression of bcl-2. However, miR-30a-5p inhibitor showed the opposite effect with regard to the degree of oxidative damage and apoptosis in H/R-induced HK-2 cells. Silencing GLUD1 rescued the influence of miR-30a-5p inhibitor on oxidative injury and apoptosis in HK-2 cells stimulated with H/R. These results demonstrated that under H/R conditions, miR-30a-5p can reduce oxidative stress in vitro by targeting GLUD1, which may be a novel therapeutic target for liver failure and worth further study.

Alzheimer's disease (AD) is a multifactorial and severe neurodegenerative disorder characterized by progressive memory decline, the presence of A beta plaques and tau tangles, brain atrophy, and neuronal loss. Available therapies provide moderate symptomatic relief but do not alter disease progression. This study demonstrated that PaPE-1, which has been designed to selectively activate non-nuclear estrogen receptors (ERs), has anti-AD capacity, as evidenced in a cellular model of the disease. In this model, the treatment of mouse neocortical neurons with A beta (5 and 10 mu M) induced apoptosis (loss of mitochondrial membrane potential, activation of caspase-3, induction of apoptosis-related genes and proteins) accompanied by increases in levels of reactive oxygen species (ROS) and lactate dehydrogenase (LDH) as well as reduced cell viability. Following 24 h of exposure, PaPE-1 inhibited A beta-evoked effects, as shown by reduced parameters of neurotoxicity, oxidative stress, and apoptosis. Because PaPE-1 downregulated A beta-inducedFas/FAS expression but upregulated that of A beta-inducedFasL, the role of PaPE-1 in controlling the external apoptotic pathway is controversial. However, PaPE-1 normalized A beta-induced loss of mitochondrial membrane potential and restored the BAX/BCL2 ratio, suggesting that the anti-AD capacity of PaPE-1 particularly relies on inhibition of the mitochondrial apoptotic pathway. These data provide new evidence for an anti-AD strategy that utilizes the selective targeting of non-nuclear ERs with PaPE-1.