Publications by authors named "Xiao-xia Kong"

To investigate the effects of Apelin-13 on barrier function injury of human umbilical vein endothelial cells (HUVECs) induced by LPS. The HUVECs cultured were divided into 4 groups: Control group, LPS group, Apelin-13+LPS group, Apelin-13 group. HUVECs were treated by 5 μg/ml LPS for 24 h to replicate the model with endothelial barrier impaired.

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Objectives: To investigate the role of autophagy inhibitor chloroquine (CQ) in acute ethanol-induced liver injury and its mechenism.

Methods: Twenty-one C57BL/6 male mice were randomly divided into three groups:control group, ethanol group, CQ + ethanol group (=7). Mice in ethanol group were administered 33% (v/v) ethanol at a dose of 4.

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Background: Although the mechanisms and pathways mediating ARDS have been studied extensively, less attention has been given to the mechanisms and pathways that counteract injury responses. This study found that the apelin-APJ pathway is an endogenous counterinjury mechanism that protects against ARDS.

Methods: Using a rat model of oleic acid (OA)-induced ARDS, the effects of ARDS on apelin and APJ receptor expressions and on APJ receptor binding capacity were examined.

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Article Synopsis
  • The endoplasmic reticulum (ER) is important for brain health, and when it gets stressed, it can lead to problems in various nervous system diseases like Alzheimer's and Parkinson's.
  • When proteins inside the ER don’t fold correctly, it can cause a response that affects neurons, especially if there isn’t enough energy.
  • Finding ways to fix the ER's problems might help create new treatments or medicines for these neurological diseases in the future.
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Objective: To investigate the role of autophagy inhibitor chloroquine (CQ) in the proliferation of pulmonary arterial smooth muscle cells (PASMCs) in hypoxia conditions.

Methods: The following groups in this study were set up: control group, hypoxia group, 50 micromol/L CQ + hypoxia group, 50 micromol/L CQ group. The viability of PASMCs in every group was detected by MTT assay.

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Objective: To observe the change of apelin and its receptor (APJ) in the lung tissue of rats with pulmonary hypertension induced by monocrotaline and to explore its significance.

Methods: Twenty-five male SD rats were randomly divided into control group (n = 10) and monocrotaline group (n = 15). On the twenty-first day after the rats were intraperitoneally injected 60 mg/kg monocrotaline for monocrotaline group or equal volume vehicle for control group, the mean pulmonary artery pressure was measured by right heart catheterization.

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The role of autophagy in the recovery of spinal cord injury remains controversial; in particular, the mechanism of autophagy regulated degradation of ubiquitinated proteins has not been discussed to date. In this study, we investigated the protective role of basic fibroblast growth factor (bFGF) both in vivo and in vitro and demonstrated that excessive autophagy and ubiquitinated protein accumulation is involved in the rat model of trauma. bFGF administration improved recovery and increased the survival of neurons in spinal cord lesions in the rat model.

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Objective: To investigate the time order of autophagy and apoptosis in human U251 cells injury after H2O2 treatment.

Methods: 4 groups in this study were set up, normal control group, 1 mmol/L H2O2 (6 h,12 h, 24 h) group. The viability of U251 cells treated with H2O2 was measured by MTT assay.

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Article Synopsis
  • The study aimed to understand how endoplasmic reticulum stress causes cell death in the lungs of rats with hypoxic pulmonary hypertension.
  • The research found significant increases in pulmonary arterial pressure and right ventricle weight ratio in hypoxic rats, along with a higher number of apoptotic cells in lung tissue compared to control rats.
  • There was also a notable upregulation of specific proteins and gene expressions related to stress responses in the pulmonary tissue of the hypoxic group, indicating a potential link between endoplasmic reticulum stress and the observed apoptosis.
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Oxidative stress could induce apoptosis and autophagy process simultaneously, but the role of autophagy is still not clear. Beclin 1, a key gene regulating the preautophagosome formation, is involved in the injury induced by oxidative stress. To observe the role of autophagy in H2O2-induced injury of U251 cells, the recombinant plasmid Psilencer3.

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The pool of ovarian primordial follicles is established during embryonic development or at birth. During the development from primordial to primary, secondary, and antral follicles, only a small portion of follicles can mature and successfully ovulate; the others are destined to degenerate through apoptotic or atretic loss. As aging advances, females ultimately enter the cessation phase of the estrous cycle and are no longer capable of fertilization.

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Recently, studies reported that neonatal genistein treatment inhibited breakdown of oocyte nests and increased oocyte survival, resulting in multi-oocyte survival in adult mice. However, whether the inhibition effect in ovarian follicular development exists also in other stages during ovarian development (e.g.

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