Rabbit Anti-Human LAMP2 (a.a. 301-411) Polyclonal antibody

Background: Pyrroloquinoline quinone is an anionic, water-soluble compound with antioxidant characteristic. The role of pyrroloquinoline quinone in pharmacology and nutrition has attracted wide attention of researchers. Although a few experiments have confirmed that pyrroloquinoline quinone plays an obvious effective role in neuroprotection. There are few reports about the effect of pyrroloquinoline quinone on traumatic brain injury. Traumatic brain injury is one of the leading causes for adult disability and death. So far, there are no effective treatment methods for the injury because of its complex pathophysiology. Method: In the present study, a model of traumatic brain injury in rat was established to study the role of pyrroloquinoline quinone in central nervous system injury. Results: The results showed that the protein expression of cleaved-Caspase 3/Caspase 3 increased after traumatic brain injury and the expression decreased by treatment with 2mM pyrroloquinoline quinone. Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining displayed that the TUNEL positive signals were up-regulated after traumatic brain injury and were down-regulated after treatment with 2mM pyrroloquinoline quinone. The protein expression of LC3II/LC3I or lysosome-associated membrane protein 2(LAMP2) was elevated after traumatic brain injury and reduced after administration with 2mM pyrroloquinoline quinone. Transmission electron microscopy showed that the number of autophagosomes increased markedly after traumatic brain injury and decreased on administration of 2mM pyrroloquinoline quinone. Electroencephalogram indicated that pyrroloquinoline quinone improved brain electrophysiological function after traumatic brain injury. The results of CCK-8 test showed that pyrroloquinoline quinone could increase the viability of primary astrocyte treated with Glutamate. Lactate dehydrogenase (LDH) assay demonstrated that pyrroloquinoline quinone decreased LDH content in primary astrocyte exposed to Glutamate. Conclusion: Pyrroloquinoline quinone could play a neuroprotective role after traumatic brain injury in rat, which might be associated with inhibiting apoptosis and autophagy caused by traumatic brain injury.

We previously reported that moderate hypoxia and hypoxia-mimetic agents including cobalt chloride (CoCl2) induce differentiation of human acute myeloid leukemia (AML) cells through hypoxia-inducible factor-I alpha (HIF-1 alpha), which interacts with and enhances transcriptional activity of CCAAT-enhancer binding factor alpha and Runx1/AML1, two important transcriptional factors for hematopoietic cell differentiation. Here, we show that autophagy inhibitor chloroquine (CQ) increases HIF-1 alpha accumulation, thus potentiating CoCl2-induced growth arrest and differentiation of leukemic cells. Furthermore, the increased effect of CQ on differentiation induction is dependent of the inhibition of autophagosome maturation and degradation, since this sensitization could be mimicked by the suppression of expression of both lysosome-associated membrane proteins 1 and 2 (LAMP1 and LAMP2). These findings not only provide the evidence that CQ is a sensitizer for CoCl2-induced differentiation of leukemic cells but also possibly propose the new therapeutic strategy for differentiation induction of AML. (C) 2012 Elsevier Inc. All rights reserved.