HS protects rat cerebral ischemia-reperfusion injury by inhibiting expression and activation of hippocampal ROCK at the Thr436 and Ser575 sites.

Background: HS is an endogenous gas signal molecule, which protects cerebral ischemia/reperfusion (I/R) injury by phosphorylating rho-associated coiled coil-containing protein kinase 2 (ROCK) at Tyr722, and inhibiting ROCK protein expression and activities. We previously reported that HS protected rat neurons from hypoxia/reoxygenation injury in vitro through inhibiting phosphorylation of ROCK at Thr436 and Ser575, but it is unclear whether these two sites are involved in protection of HS against cerebral I/R injury.

Method: Rats transfected with wild-type and mutant eukaryotic plasmids of ROCK in hippocampus were used to establish I/R model by ligating bilateral common carotid artery.

Endothelium-derived hydrogen sulfide acts as a hyperpolarizing factor and exerts neuroprotective effects via activation of large-conductance Ca -activated K channels.

Background And Purpose: Endothelium-derived hyperpolarizing factor (EDHF) has been suggested as a therapeutic target for vascular protection against ischaemic brain injury. However, the molecular entity of EDHF and its action on neurons remains unclear. This study was undertaken to demonstrate whether the hydrogen sulfide (H S) acts as EDHF and exerts neuroprotective effect via large-conductance Ca -activated K (BK /K 1.

3-Mercaptopyruvate sulfurtransferase/hydrogen sulfide protects cerebral endothelial cells against oxygen-glucose deprivation/reoxygenation-induced injury via mitoprotection and inhibition of the RhoA/ROCK pathway.

3-Mercaptopyruvate sulfurtransferase (3-MST) is the major source of hydrogen sulfide (HS) production in the brain and participates in many physiological and pathological processes. The present study was designed to investigate the role of 3-MST-derived HS (3-MST/HS) on oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cerebrovascular endothelial cells (ECs). Using cerebrovascular specimens from patients with acute massive cerebral infarction (MCI), we found abnormal morphology of the endothelium and mitochondria, as well as decreases in HS and 3-MST levels.

Mechanism of HS-mediated ROCK inhibition of total flavones of against myocardial ischemia injury.

Our previous studies have indicated that pretreatment with total flavones of flower (TFR) may protect against myocardial ischemic injuries in rats and mice. The cystathionine γ-lyase/hydrogen sulfide (CSE/HS) pathway have been associated with several cardiovascular diseases, but the effect of TFR on the Rho-associated protein kinase (ROCK) and CSE/HS signaling pathways remains unknown. In the present study, the protective effects of TFR as a ROCK inhibitor in a mice model of myocardial infarction induced by isoproterenol (ISO) were investigated, and the hearts from the wild type and CSE knockout (KO) mice were examined.

Total flavones of Rhododendron simsii Planch flower protect rat hippocampal neuron from hypoxia-reoxygenation injury via activation of BK channel.

Objectives: To study the effects of total flavones of Rhododendra simsii Planch flower (TFR) on hypoxia/reoxygenation (H/R) injury in rat hippocampal neurons and its underlying mechanism.

Method: Model of H/R was established in newborn rat primary cultured hippocampal neuron. Lactate dehydrogenase (LDH) and neuron-specific enolase (NSE) activity as well as malondialdehyde (MDA) content in cultured supernatants of the neurons were examined.

Urotensin-#receptor antagonist SB-706375 protected isolated rat heart from ischaemia-reperfusion injury by attenuating myocardial necrosis via RhoA/ROCK/RIP3 signalling pathway.

SB-706375 is a selective receptor antagonist of human urotensin-II (hU-II), which can block the aorta contraction induced by hU-II in rats. The effect of SB-706375 on myocardial ischaemia-reperfusion (I/R) injury is unclear. The major objective of this study was to investigate whether SB-706375 has a protective effect on myocardial I/R injury in rats and explore its possible mechanisms.

Spinal NGF induces anti-intrathecal opioid-initiated cardioprotective effect via regulation of TRPV1 expression.

Evidences from previous studies confirmed that intrathecal morphine preconditioning (ITMP) reduces the cardiac injury of ischemia-reperfusion (IR) via the central nervous system. However, the molecular mechanism is not fully understood. The breath of central nerve growth factor (NGF) during nociceptive transmission has been well documented, and little is known about the significance of NGF in myocardial injury of IR and intrathecal morphine-induced cardioprotection.

Role of CSE-Produced HS on Cerebrovascular Relaxation via RhoA-ROCK Inhibition and Cerebral Ischemia-Reperfusion Injury in Mice.

The role of CSE-produced HS on cerebrovascular relaxation and cerebral ischemia-reperfusion (I/R) injury was investigated using CSE knockout (CSE) and wild-type (CSE) mice. The relaxation of the cerebral basilar artery (BA) to CSE-produced HS and its mechanism were detected. The results revealed that both NaHS, a donor of exogenous HS, and ROCK inhibitor Y27632 could induce significant relaxation of the BA, but the relaxation of the BA to NaHS was significantly attenuated by Y27632.

Total Flavone of Rhododendron Improves Cerebral Ischemia Injury by Activating Vascular TRPV4 to Induce Endothelium-Derived Hyperpolarizing Factor-Mediated Responses.

Background: Total flavonoids of Rhododendron (TFR) is extracted from Rhododendron, a herbal medicine widely used in China. The main components are flavone compounds such as warfarin, rutin, quercetin, and hyperoside. We investigated the role of TRPV4 channel in the TFR induced endothelium-dependent hyperpolarizing factor- (EDHF-) mediated responses against ischemia/reperfusion injury (IR) in cerebral IR (CIR) rats.

Vascular Protection of Hydrogen Sulfide on Cerebral Ischemia/Reperfusion Injury in Rats.

This study was undertaken to demonstrate the vascular protection of exogenous and endogenous hydrogen sulfide (HS) on cerebral ischemia/reperfusion (I/R) injury. The effect of HS on cerebrovascular dysfunction in middle cerebral artery (MCA) and neuronal damage were measured after cerebral I/R induced by transient middle cerebral artery occlusion (MCAO) in cystathionine c-lyase (CSE) knockdown and wild-type rats. The effect of sodium hydrosulfide (NaHS, donor of exogenous HS), L-cysteine (L-Cys, substrate of endogenous HS), and endothelium cells on the responses of isolated MCA derived from non-ischemic rats was also evaluated to assess the underlying mechanism of HS-mediate cerebral vasodilation.

Total flavones of Rhododendron simsii Planch flower protect isolated rat heart from ischaemia-reperfusion injury and its mechanism of UTR-RhoA-ROCK pathway inhibition.

Objectives: Total flavones of Rhododendron simsii Planch flower (TFR) are an effective part extracted from the flower. The present study was designed to investigate the protective effect of TFR in isolated rat heart following global ischaemia-reperfusion and the possible underlying mechanisms.

Methods: Langendorff perfusion apparatus was used to perfuse isolated rat heart which was subjected to global ischaemia-reperfusion.

Particular Levels of Odors Released by Virgin Females Attract Conspecific Males of the Funnel-Web Spider Allagelena difficilis.

Female-released chemical signals are crucial clues for mate-searching males to locate and gain sexual receptivity of conspecific females. Abundant behavioral evidence indicates that female spiders release sex pheromones to guide mate-searching behavior of conspecific mature males. However, the chemical nature of spider pheromones is poorly understood.

Total Flavones of Planch Flower Protect against Cerebral Ischemia-Reperfusion Injury via the Mechanism of Cystathionine--Lyase-Produced HS.

Total flavones of Planch flower (TFR) have a significant protective effect against cerebral ischemia-reperfusion injury. However, its mechanism is unclear. This study investigated the protection of TFR against cerebral ischemia-reperfusion injury via cystathionine--lyase- (CSE-) produced HS mechanism.

miR‑133b‑5p contributes to hypoxic preconditioning‑mediated cardioprotection by inhibiting the activation of caspase‑8 and caspase-3 in cardiomyocytes.

In a previous study using a microRNA (miRNA/miR) microarray assay, we demonstrated that miR-133b-5p was upregulated in response to hypoxic preconditioning (HPC). The present study was designed to investigate the role of the miR‑133b‑5p in HPC‑induced cardioprotection and the underlying mechanisms involving caspase‑8 and caspase‑3 apoptotic signaling. Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR‑133b‑5p in myocardium was measured.

The Protective Effect of Total Flavones from Planch. on Myocardial Ischemia/Reperfusion Injury and Its Underlying Mechanism.

Objectives: Total flavones from Planch. (TFR) are the effective part extracted from the flowers of Planch. and have obvious protective effects against cerebral ischemic or myocardial injuries in rabbits and rats.

[Quality of realgar and its influencing factors based on toxicity].

The results of a toxicity analysis showed differences from those of the existing experimental data. Therefore, HPLC-ICP-MS was used to analyze the soluble arsenic content at different valences in realgar prepared with water grind processing, which were collected from 3 companies. The results showed that the free arsenic of the 3 companies did not exceed the limit of Chinese Pharmacopoeia.

Anfibatide protects against rat cerebral ischemia/reperfusion injury via TLR4/JNK/caspase-3 pathway.

Anfibatide (ANF) is a GPIb antagonist derived from the protein complex agglucetin. Previous studies have showed that it has protective effect on cerebral ischemia/reperfusion injury, the mechanism of which is still unclear, however. The present study was designed to investigate the protective effect of ANF on cerebral I/R injury in rats and the possible mechanisms.

Sufentanil attenuates impairment of the endothelium-dependent vasodilation induced by hypoxia-reoxygenation in the rat coronary artery.

Sufentanil has been used broadly in cardiac surgery, but the mechanisms by which it modulates coronary vascular tone after ischemia-reperfusion injury are largely unknown. Effects of sufentanil on coronary tone and on the relaxation of rat coronary arteries (CAs) in response to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) relaxing agents in the presence of hypoxia-reoxygenation (H/R) was studied in an in vitro organ chamber setup. Sufentanil (10-10 mol/L) relaxed rat CA rings in endothelium-dependent and endothelium-independent manners.

Urotensin-ⅡReceptor Antagonist SB-710411 Protects Rat Heart against Ischemia-Reperfusion Injury via RhoA/ROCK Pathway.

Aim: SB-710411 is a rat selective urotensin-II (U-II) receptor antagonist, which can block U-II-induced contraction of the aorta and inhibit U-II-induced myocardial fibrosis in rats. However, the effect of SB-710411 on myocardial ischemia-reperfusion (I/R) injury is unclear. The present study was designed to investigate whether SB-710411 has a protective effect on myocardial I/R injury in rats and the possible mechanisms.

Acid-sensing ion channel 1a contributes to the effect of extracellular acidosis on NLRP1 inflammasome activation in cortical neurons.

Background: Acid-sensing ion channels (ASICs) are cation channels which were activated by extracellular acidosis and involved in various physiological and pathological processes in the nervous system. Inflammasome is a key component of the innate immune response in host against harmful and irritable stimuli. As the first discovered molecular platform, NLRP1 (nucleotide-binding oligomerization domain (NOD)-like receptor protein 1) inflammasome is expressed in neurons and implicated in many nervous system diseases such as brain injury, nociception and epilepsy.

[Protective effect against myocardial ischemia reperfusion injuries induced by hyperoside preconditioning and its relationship with PI3K/Akt signaling pathway in rats].

To investigate the protective effect of preconditioning with hyperoside ( Hyp) against myocardial ischemia-reperfusion injury (MIRI) in rats and the role of PI3K/Akt signaling pathway. MIRI was established by ligation of left anterior descending coronary artery for 30 min followed by reperfusion for 120 min in rats. Male SD rats were randomly divided into five groups: sham group,model group (MIRI),Hyp preconditioning group(Hyp), Hyp preconditioning + LY294002 (a PI3K/Akt signaling pathway inhibitor) group (Hyp + LY), and LY294002 group (LY).

[Effects and mechanisms of hyperoside on vascular endothelium function in middle cerebral arteries of rats ex vivo].

To investigate the effects and potential mechanisms of hyperoside (Hyp) on the vascular endothelium function in middle cerebral artery (MCA) ex vivo in rats. Isolated arterial segments from MCAs of rats were used for surveying vasomotoricity in a pressurized chamber. Transmembrane potential was recorded by using glass microelectrodes to evaluate hyperpolarization.

[Preparation and luminescent properties of light scattering fluorescent resin].

With the methods of compound-melting and high-temperature molding, PC/YAG:Ce fluorescent resin pieces were prepared. The transmittance of the prepared PC/YAG:Ce fluorescent resin in 500~800 nm reaches approximately 65% (0.71 mm thick, double sides polished).

Protective Effect and Mechanism of Total Flavones from Rhododendron simsii Planch Flower on Cultured Rat Cardiomyocytes with Anoxia and Reoxygenation.

Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones from Rhododendron simsii Planch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown.