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.

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.

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.

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.

Protective effect of pharmacological preconditioning of total flavones of abelmoschl manihot on cerebral ischemic reperfusion injury in rats.

The present study was to investigate the effect of pharmacological preconditioning of total flavones of abelmoschl manihot (TFA) on cerebral ischemic reperfusion injury in rats. Rat cerebral ischemia/reperfusion injury was induced by occluding the right middle cerebral artery (MCA). The infarct size was determined by staining with 2,3,5-triphenyl tetrazalium chloride (TTC).

[Preliminary study on the ecology of Trichobilharzia cercariae in the Huaihe river system].

Objective: To investigate the ecological habit and characteristics of Trichobilharzia cercariae in the Huaihe river system.

Methods: During June of 2002-May of 2003, Radix auricularia snails were collected monthly in Yaohe Fishery of the branch of the Huaihe River. The cercariae, released from the positive snails and collected by Shade Drop Bottle, were examined by direct press.