The mineralocorticoid receptor-p38MAPK-NFκB or ERK-Sp1 signal pathways mediate aldosterone-stimulated inflammatory and profibrotic responses in rat vascular smooth muscle cells.

Aim: To explore the signalling pathways involved in aldosterone-induced inflammation and fibrosis in rat vascular smooth muscle cells (VSMCs).

Methods: Using Western blotting and real-time RT-PCR, we investigated the effects of aldosterone on the expression of cyclooxygenase-2 (Cox-2) and IL-6, two important proinflammatory factors, and TGFβ1, a critical profibrotic factor, in VSMCs.

Results: Aldosterone treatment significantly increased the expression of Cox-2 and IL-6 and activation of p38MAPK and NF-κB.

Inhibition of methamphetamine-induced apoptosis by the calcium channel blocker verapamil in rat cerebellar neurons.

Objective: To study protective effects of verapamil on neurotoxicity induced by methamphetamine (MA) in rat cerebellar neuronal cells (R2 cells) and explore the possible mechanisms.

Methods: MA neurotoxicity to R2 cells was examined by MTT reduction and LDH leakage assays. Using flow cytometer and agarose gel electrophoresis, apoptosis induced by MA in R2 cells was observed.

Nerve growth factor protects R2 cells against neurotoxicity induced by methamphetamine.

It is well known that methamphetamine is a neurotoxic drug of abuse to cause cell death both in vitro and in vivo. In this study, the protective effect of nerve growth factor on methamphetamine-induced neurotoxicity was examined in R2 cells. Treatment of R2 cells with methamphetamine for 48 h induced apoptotic-like death as determined by cell viability assay, DNA fragmentation on agarose gel and flow cytometric analysis.