[Effects of CHL1 deficiency,a cell adhesion molecule,on the inflammatory bowel disease].

Objective: To investigate the effects of deficiency of CHL1 in inflammatory bowel disease (IBD).

Methods: Dextran Sulfate Sodium (DSS)-induced colitis model was used to study the effects of deficiency of CHL1 on the development of IBD. Ten CHL1(+/+) mice in C57/BL6 background were randomly divided into CHL1(+/+) group and DSS-induced CHL1(+/+) group.

miR-210 protects renal cell against hypoxia-induced apoptosis by targeting HIF-1 alpha.

The kidney is vulnerable to hypoxia-induced injury. One of the mechanisms underlying this phenomenon is cell apoptosis triggered by hypoxia-inducible factor-1-alpha (HIF-1α) activation. MicroRNA-210 (miR-210) is known to be induced by HIF-1α and can regulate various pathological processes, but its role in hypoxic kidney injury remains unclear.

Methylene Blue Reduces Acute Cerebral Ischemic Injury via the Induction of Mitophagy.

The treatment of stroke is limited by a short therapeutic window and a lack of effective clinical drugs. Methylene blue (MB) has been used in laboratories and clinics since the 1890s. Few studies have reported the neuroprotective role of MB in cerebral ischemia-reperfusion injury.

Enhanced hypoxia-inducible factor (HIF)-1α stability induced by 5-hydroxymethyl-2-furfural (5-HMF) contributes to protection against hypoxia.

We first reported the role of 5-hydroxymethyl-2-furfural (5-HMF) against hypoxia. Here, we studied the mechanism by using oxygen-dependent degradation domain (ODD)-Luc mice, which are a useful model to probe the stabilization of hypoxia-inducible factor 1α (HIF-1α). Compared with three other compounds that have been reported to have a role in stabilizing HIF-1α, 5-HMF caused stronger bioluminescence, which is indicative of HIF-1α stability in the brain and kidney of ODD-Luc mice.

[Effect of high altitude hypoxia on cognitive flexibility].

Objective: To explore the effects of high altitude on cognitive flexibility.

Methods: Simulated hypoxia at an altitude of 3 600 m was performed in a hypobaric chamber. Twenty-three volunteers without hypoxic experience were selected and the mean age was about 25.

[The effects of autophagy on cell survival under different hypoxia].

Objective: To investigate the regulation of different hypoxia on cell survival and autophagy.

Methods: PC12 cells were treated with different hypoxia. The cell survival was measured by MTT assay, expressions of LC3 and p62 were marked for autophagy detected by Western Blot, and the level of reactive oxygen species (ROS) was analyzed by flow cytometry.

[Influence of acute hypoxia on CHL1 expression in different tissues of mice].

Objective: To observe the effects of acute hypoxia on the cell adhesion molecule close homologue of L1 (CHL1) expression in different brain areas and main organs (heart, lung, kidney) of mice, and provide a basis for the role of CHL1 in hypoxia injury.

Methods: Mice were randomly divided into two groups (n=10): normoxia group and hypoxia group. Hypoxia group were treated by acute hypoxia (8% O2, 8 h).

Loss of NB-3 aggravates cerebral ischemia by impairing neuron survival and neurite growth.

Background And Purpose: NB-3 is a member of the F3/contactin family of neural recognition molecules, which are crucial for cell morphogenesis and motility. NB-3 is expressed in neurons and plays an important role in axonal extension and neuronal survival. However, the role of NB-3 in cerebral ischemic injury remains unknown.

The protective role of 5-hydroxymethyl-2-furfural (5-HMF) against acute hypobaric hypoxia.

Our previous study showed that pretreatment with 5-hydroxymethyl-2-furfural (5-HMF) led to protection against hypoxic injury via a p-ERK-mediated pathway in vitro. Whether the protection of 5-HMF against hypoxia is effective in vivo is unknown. The present study is aimed to verify the role of 5-HMF in acute hypobaric hypoxia using Kunming mice as an in vivo model and further investigate the underlying mechanisms.

Gene expression profiles and metabolic changes in embryonic neural progenitor cells under low oxygen.

Hypoxia promotes the proliferation of neural progenitor cells (NPCs), and low oxygen is a useful tool for expansion of NPCs in vitro. To further understand the regulation of the mechanisms involved, we first identified the gene expression profile of NPCs and characterized their metabolic changes in vitro under 3% oxygen. NPCs derived from E13.

[Effect of low glucose and/or hypoxia on the proliferation and metabolism of neural stem cells].

Objective: Recent study demonstrated that hypoxia could regulate the proliferation and differentiation of neural stem cells in vitro. In the present study, effects of low glucose and/or hypoxia on the proliferation and metabolism of neural stem cells were investigated in vitro.

Methods: The neural stem cells were isolated from the rat embryonic mesencephalon (E13.

CHL1 negatively regulates the proliferation and neuronal differentiation of neural progenitor cells through activation of the ERK1/2 MAPK pathway.

Neural recognition molecules of the immunoglobulin superfamily play important roles in the development and regeneration of nervous system. Close Homologue of L1 (CHL1) is a member of the L1 family of recognition molecules which are expressed during neuronal development, suggesting a potential role in neural progenitor cells (NPCs). Here, we investigated the role of CHL1 in the proliferation and differentiation of NPCs both in vivo and in vitro, and the possible mechanism involved.