Hydrogen sulfide antagonizes formaldehyde-induced ferroptosis via preventing ferritinophagy by upregulation of GDF11 in HT22 cells.

Formaldehyde (FA) has neurotoxic characteristics and causes neurodegenerative disease. Our previous study demonstrated the neuroprotective effects of hydrogen sulfide (HS) on FA-induced neurotoxicity in HT22 cells. Emerging evidence have supported that ferroptosis is involved in FA-induced neurotoxicity.

Pathogen distribution and bacterial resistance in children with severe pneumonia: A single-center retrospective study.

To examine the etiological distribution of pathogens in pediatric patients with severe pneumonia and analyze the drug resistance of major pathogen species.Nasopharyngeal secretion specimens were collected for bacterial culture from pediatric patients admitted to the Xiamen children's hospital who were diagnosed with severe pneumonia from January 2016 to December 2019. Pathogen species were detected by quantitative polymerase chain reaction, direct immunofluorescence, and bacterial culture and we examined the drug susceptibility of the bacterial pathogens.

Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux Up-regulation of SIRT1.

Hyperglycemia, a key characteristic and risk factor for diabetes mellitus (DM), causes neuronal senescence. Hydrogen sulfide (HS) is a novel neuroprotectant. The present work was to investigate the potential effect of HS on hyperglycemia-induced neuronal senescence and the underlying mechanisms.

Genistein Protects H9c2 Cardiomyocytes against Chemical Hypoxia-Induced Injury via Inhibition of Apoptosis.

Background/aims: Hypoxia can induce cell injury in cardiomyocytes and further lead to cardiovascular diseases. Genistein (Gen), the predominant isoflavone found in soy products, has shown protective effects on cardiovascular system. The aim of the present study was to investigate the cardioprotective effect of Gen against chemical hypoxia-induced injury.

BDNF/TrkB Pathway Mediates the Antidepressant-Like Role of HS in CUMS-Exposed Rats by Inhibition of Hippocampal ER Stress.

Our previous works have shown that hydrogen sulfide (HS) significantly attenuates chronic unpredictable mild stress (CUMS)-induced depressive-like behaviors and hippocampal endoplasmic reticulum (ER) stress. Brain-derived neurotrophic factor (BDNF) generates an antidepressant-like effect by its receptor tyrosine protein kinase B (TrkB). We have previously found that HS upregulates the expressions of BDNF and p-TrkB in the hippocampus of CUMS-exposed rats.

Fabrication and characterization of a novel self-assembling micelle based on chitosan cross-linked pectin-doxorubicin conjugates macromolecular pro-drug for targeted cancer therapy.

Cancer is one of the leading causes of morbidity and mortality worldwide. Doxorubicin is one of the most effective anticancer drugs approved by FDA. However, like all the other anticancer drugs, the efficacy of DOX is associated with high systemic toxicity to healthy tissues.

Inhibition of ALDH2 protects PC12 cells against formaldehyde-induced cytotoxicity: involving the protection of hydrogen sulphide.

Formaldehyde (FA), a common environmental contaminant, has toxic effects on the central nervous system (CNS). We have previously found that hydrogen sulphide (H S), the third endogenous gaseous mediator, protects neuron against the toxicity of FA. However, the underlying mechanism is poor.

Adsorption kinetics, isotherms and thermodynamics of atrazine on surface oxidized multiwalled carbon nanotubes.

The adsorption kinetics, isotherms and thermodynamic of atrazine on multiwalled carbon nanotubes (MWCNTs) containing 0.85%, 2.16%, and 7.

Heat shock protein 90 acts as a molecular chaperone in late-phase activation of extracellular signal-regulated kinase 1/2 stimulated by oxidative stress in vascular smooth muscle cells.

Aim: To investigate whether cytosolic heat shock protein 90 (HSP90) acts as a molecular chaperone on the activated extracellular signal-regulated kinase 1/2 (ERK1/2) and cell proliferation stimulated by reactive oxygen species (ROS) in rat vascular smooth muscle cells (VSMC).

Methods: VSMC were exposed to 1 micromol/L LY83583 (6-anilinoquinoline-5,8-quinolinedione, producer of ROS) for 120 min in the presence or absence of 5 micromol/L geldanamycin, a specific inhibitor of HSP90. Then the total, soluble, and insoluble proteins of the cells were collected.

Phytoestrogen genistein supplementation increases eNOS and decreases caveolin-1 expression in ovariectomized rat hearts.

This study examined whether genistein influences the production of nitric oxide (NO) and expression of endothelial nitric oxide synthase (eNOS) and the modulators of eNOS activity in ovariectomized (OVX) rat hearts. Female mature Sprague-Dawley rats were subjected to bilateral ovariectomy, OVX rats were randomly divided into four groups: 17beta-estradiol (0.1 mg/kg, s.

Identification of peptides inhibiting adhesion of monocytes to the injured vascular endothelial cells through phage-displaying screening.

Using oxidized low-density lipoprotein (LDL)-injured vascular endothelial cells (ECs) as target cells, peptides specifically binding to the injured ECs were screened from a phage-displaying peptide library by using the whole-cell screening technique after three cycles of the adsorption-elution-amplification procedure. Positive phage clones were identified by ELISA, and the inserted amino acid sequences in the displaying peptides were deduced from confirmation with DNA sequencing. The adhesion rate of ECs to monocytes was evaluated by cell counting.

Onychin inhibits proliferation of vascular smooth muscle cells by regulating cell cycle.

Aim: To investigate the effects of onychin on the proliferation of cultured rat artery vascular smooth muscle cells (VSMCs) in the presence of 10% new-born calf serum (NCS).

Methods: Rat VSMCs were incubated with onychin 150 micromol/L or genistein 10 micromol/L in the presence of 10% NCS for 24 h. The proliferation of VSMCs was measured by cell counting and MTS/PMS colorimetric assays.

Probucol inhibits oxidized-low density lipoprotein-induced adhesion of monocytes to endothelial cells in vitro.

Aim: To investigate the mechanism by which probucol (PBC) affected adhesion of monocytes to human umbilical vein endothelial cells (HUVEC).

Methods: Effects of PBC on expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), P-selectin, a nd E-selectin in human umbilical vein endothelial cells were examined. Moreover, the inhibitory effect of PBC were compared with that of monoclonal antibodies (mAbs) to ICAM-1, VCAM-1, P-selectin, and E-select in on adhesion induced by oxidized-low density lipoprotein(Ox-LDL).