SCM-198 inhibits microglial overactivation and attenuates Aβ(1-40)-induced cognitive impairments in rats via JNK and NF-кB pathways.

Background: Neuroinflammation mediated by overactivated microglia plays a key role in many neurodegenerative diseases, including Alzheimer's disease (AD). In this study, we investigated for the first time the anti-neuroinflammatory effects and possible mechanisms of SCM-198 (an alkaloid extracted from Herbaleonuri), which was previously found highly cardioprotective, both in vitro and in vivo.

Methods: For in vitro experiments, lipopolysaccharide (LPS) or β-amyloid(1-40) (Aβ(1-40)) was applied to induce microglial overactivation.

A new hope for neurodegeneration: possible role of hydrogen sulfide.

For hundreds of years, hydrogen sulfide (H2S) has been known solely as a toxic gas with the smell of rotten eggs. Nevertheless, the notoriety of H2S as a toxic gas is experiencing a transformation, with an increasing amount of research showing that it regulates a range of physiological and pathological processes in mammals. Hence H2S is a physiologically important molecule and has been referred to as the third gaseous mediator alongside nitric oxide and carbon monoxide.

Neuroprotective effects of SCM198 on 6-hydroxydopamine-induced behavioral deficit in rats and cytotoxicity in neuronal SH-SY5Y cells.

6-Hydroxydopamine (6-OHDA), one of the most investigated Parkinson's disease neurotoxins, is widely used to study mechanisms of cell death in dopaminergic neurons. In the present study, we demonstrated that SCM198, a new compound based on the active component of Herba leonuri, significantly reduced 6-OHDA-induced cell death in dopaminergic SH-SY5Y cells and attenuated apomorphine-elicited rotational behavior in 6-OHDA-lesioned rats. Pretreatment with SCM198 (0.

Kir6.2 knockout alters neurotransmitter release in mouse striatum: an in vivo microdialysis study.

ATP-sensitive potassium (K-ATP) channels have been demonstrated to play important roles in the brain. In the present study, Kir6.2 knockout (Kir6.

ATP-sensitive potassium channel opener iptakalim protected against the cytotoxicity of MPP+ on SH-SY5Y cells by decreasing extracellular glutamate level.

Mounting evidence reveals that ATP-sensitive potassium (K(ATP)) channel openers (KCOs) exert significant neuroprotection in vivo and in vitro in several models of Parkinson's disease (PD). However, the mechanisms are not well understood. In this study, we demonstrated that SH-SY5Y cells expressed mRNA and proteins for Kir6.