[Comprehensive intervention combined with cognitive psychological care based on quality chain for patients with benign prostatic hyperplasia].

Objective: To investigate the application effect of comprehensive intervention combined with cognitive psychological care based on the quality chain in patients with BPH.

Methods: We prospectively selected 110 cases of BPH treated in our hospital from January 2022 to March 2023 and equally randomized them into groups A and B, the former given routine intervention, while the latter comprehensive intervention combined with cognitive psychological care based on the quality chain in addition. We analyzed the results of intervention, the patients' scores on Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS), improvement of clinical indicators, self-efficacy, disease awareness and treatment compliance, and compared the data obtained between the two groups of patients.

The cytoprotective role of omentin against oxidative stress-induced PC12 apoptosis.

Oxidative stress has been proven to play a critical role in the pathogenesis of neuronal injury. As a novel adipocytokine, omentin is produced by visceral adipose with insulin sensitizing effects and has been revealed to possess anti-inflammatory effects. However, the possible effect of omentin on oxidative stress remains unknown.

GCN2 suppression attenuates cerebral ischemia in mice by reducing apoptosis and endoplasmic reticulum (ER) stress through the blockage of FoxO3a-regulated ROS production.

Ischemic stroke is one of the leading causes of morbidity and mortality among human worldwide. Unfortunately, cerebral I/R still lacks effective therapeutic targets and strategies. In the study, we found that general control nonderepressible 2 (GCN2) expression was increased following ischemia in the ischemic penumbra in vivo and in vitro.

Dynamin-related protein 1 inhibitors protect against ischemic toxicity through attenuating mitochondrial Ca2+ uptake from endoplasmic reticulum store in PC12 cells.

Intracellular calcium homeostasis disorder and mitochondrial dysfunction are involved in many acute and chronic brain diseases, including ischemic brain injury. An imbalance in mitochondrial fission and fusion is one of the most important structural abnormalities found in a large number of mitochondrial dysfunction related diseases. Here, we investigated the effects of mitochondrial division inhibitor A (mdivi A) and mdivi B, two small molecule inhibitors of mitochondrial fission protein dunamin-related protein 1 (Drp-1), in neuronal injury induced by oxygen-glucose deprivation (OGD) in PC12 cells.

Aggravated inflammation and increased expression of cysteinyl leukotriene receptors in the brain after focal cerebral ischemia in AQP4-deficient mice.

Objective: Aquaporin-4 (AQP4), the main water channel protein in the brain, plays a critical role in water homeostasis and brain edema. Here, we investigated its role in the inflammatory responses after focal cerebral ischemia.

Methods: In AQP4-knockout (KO) and wild-type mice, focal cerebral ischemia was induced by 30 min of middle cerebral arterial occlusion (MCAO).

Aggravated chronic brain injury after focal cerebral ischemia in aquaporin-4-deficient mice.

The water channel aquaporin-4 (AQP4) is important in brain water homeostasis, and is also involved in astrocyte growth and glial scar formation. It has been reported that AQP4 deficiency attenuates acute ischemic brain injury as a result of reducing cytotoxic edema. Here, we determined whether AQP4 deficiency influences chronic brain injury after focal cerebral ischemia induced by 30 min of middle cerebral artery occlusion (MCAO).

Aquaporin-4 deficiency attenuates acute lesions but aggravates delayed lesions and microgliosis after cryoinjury to mouse brain.

Objective: To determine whether aquaporin-4 (AQP4) regulates acute lesions, delayed lesions, and the associated microglial activation after cryoinjury to the brain.

Methods: Brain cryoinjury was applied to AQP4 knockout (KO) and wild-type mice. At 24 h and on days 7 and 14 after cryoinjury, lesion volume, neuronal loss, and densities of microglia and astrocytes were determined, and their changes were compared between AQP4 KO and wild-type mice.

[Deficiency of water channel AQP4 aggravates NMDA-induced brain injury in mice].

Objective: To evaluate the role of water channel AQP4 in NMDA-induced brain injury in mice.

Methods: In AQP4 gene knockout (AQP4(-/-)) mice, brain injury was induced by microinjection of NMDA into the cortex. The injured area was determined by toluidine blue staining, degenerated neurons were detected by Fluro-Jade B staining, and increased blood-brain barrier (BBB) permeability was evaluated by IgG immunostaining.

Montelukast, a cysteinyl leukotriene receptor-1 antagonist, attenuates chronic brain injury after focal cerebral ischaemia in mice and rats.

Objectives: Previously we demonstrated the neuroprotective effect of montelukast, a cysteinyl leukotriene receptor-1 (CysLT(1) ) antagonist, on acute brain injury after focal cerebral ischaemia in mice. In this study, we have determined its effect on chronic brain injury after focal cerebral ischaemia in mice and rats.

Methods: After transient focal cerebral ischaemia was induced by middle cerebral artery occlusion, montelukast was intraperitoneally injected in mice or orally administered to rats for five days.

CysLT2 receptor-mediated AQP4 up-regulation is involved in ischemic-like injury through activation of ERK and p38 MAPK in rat astrocytes.

Aims: We previously reported that cysteinyl leukotriene receptor 2 (CysLT(2)) mediates ischemic astrocyte injury, and leukotriene D(4)-activated CysLT(2) receptor up-regulates the water channel aquaporin 4 (AQP4). Here we investigated the mechanism underlying CysLT(2) receptor-mediated ischemic astrocyte injury induced by 4-h oxygen-glucose deprivation and 24-h recovery (OGD/R).

Main Methods: Primary cultures of rat astrocytes were treated by OGD/R to construct the cell injury model.

[Preparation and identification of polyclonal antibody against cysteinyl leukotriene receptor 2].

Objective: To prepare and identify a polyclonal antibody against cysteinyl leukotriene receptor (CysLT(2)receptor).

Methods: Rabbits were immunized with KLH-coupled CysLT(2) receptor peptide to prepare the polyclonal antibody (pAb). The titer of the pAb in rabbit plasma was detected by indirect ELISA, and the specificity of the pAb was tested by antigen blockade.

[Preparation and identification of a polyclonal antibody against novel cysteinyl leukotriene receptor GPR17].

Objective: To prepare and identify a polyclonal antibody (pAb) against GPR17, a novel cysteinyl leukotriene receptor.

Methods: Rabbits were immunized with KLH-coupled GPR17 peptide to prepare the pAb. The titer of the pAb in rabbit plasma was detected by indirect ELISA, and the specificity of the pAb was tested by antigen blockade.

Leukotriene D4 stimulates the migration but not proliferation of endothelial cells mediated by the cysteinyl leukotriene cyslt(1) receptor via the extracellular signal-regulated kinase pathway.

The actions of cysteinyl leukotrienes (CysLTs) are mediated by activating CysLT receptors, CysLT(1), and CysLT(2). The CysLT(1) receptor mediates vascular responses to CysLTs; however, its effect on the proliferation and migration of endothelial cells is not clarified. To determine this effect, we observed proliferation and migration in EA.

Activation of CysLT receptors induces astrocyte proliferation and death after oxygen-glucose deprivation.

We recently found that 5-lipoxygenase (5-LOX) is activated to produce cysteinyl leukotrienes (CysLTs), and CysLTs may cause neuronal injury and astrocytosis through activation of CysLT(1) and CysLT(2) receptors in the brain after focal cerebral ischemia. However, the property of astrocyte responses to in vitro ischemic injury is not clear; whether 5-LOX, CysLTs, and their receptors are also involved in the responses of ischemic astrocytes remains unknown. In the present study, we performed oxygen-glucose deprivation (OGD) followed by recovery to induce ischemic-like injury in the cultured rat astrocytes.

[A skilled reaching test for evaluating long-term neurological deficits after focal cerebral ischemia in mice].

Objective: To determine whether the skilled reaching test is an objective method for evaluating long-term neurological deficits after focal cerebral ischemia in mice.

Methods: In a reaching box, mice were trained to reach food pellets with their left forelimb through a 0.5 cm slit for 3 weeks.

Cilostazol, a phosphodiesterase 3 inhibitor, protects mice against acute and late ischemic brain injuries.

Cilostazol, a selective inhibitor of phosphodiesterase 3, exerts neuroprotective effects on acute brain injury after cerebral ischemia in rats. However, it is unknown whether cilostazol affects the subacute or chronic ischemic injury. In the present study, we evaluated the dose- and time-dependent effects of cilostazol on acute ischemic brain injury and the long-lasting effect on the late (subacute/chronic) injury in mice with focal cerebral ischemia induced by transient middle cerebral artery occlusion.