Neuropathic Pain Creates Systemic Ultrastructural Changes in the Nervous System Corrected by Electroacupuncture but Not by Pregabalin.

Purpose: It is unclear whether neuropathological structural changes in the peripheral nervous system and central nervous system can occur in the spared nerve injury model. In this study, we investigated the pathological changes in the nervous system in a model of neuropathic pain as well as the effects of electroacupuncture (EA) and pregabalin (PGB) administration as regards pain relief and tissue repair.

Patients And Methods: Forty adult male SD rats were equally and randomly divided into 4 groups: spared nerve injury group (SNI, n = 10), SNI with electroacupuncture group (EA, n = 10), SNI with pregabalin group (PGB, n =10) and sham-operated group (Sham, n=10).

[Angiotensin II-induced podocyte apoptosis: role of the MAPK subtypes].

Objective: To evaluate the role of the MAPK subtypes (p38MAPK, ERK and JNK) in ANG II-induced apoptosis of cultured human podocytes.

Methods: The cultured podocytes were incubated in media containing either vehicle, SB202190(5 micromol/L, an inhibitor of p38MAPK), PD98059 (1 micromol/L, an inhibitor of ERK), SP600125 (5 micromol/L, an inhibitor of JNK), ANG II (10(-8)mol/L) with or without SB202190 PD98059 and SP600125 for 18 hours; the cells were assayed for apoptosis by morphologic staining with H-33342 and propidium iodide and DNA fragmentation assays; the cell proteins were probed for phosphorylated MAPKs to determine the activation of specific MAPK subtypes.

Results: ANG II promoted podocyte apoptosis in a time- and dose-dependent manner; ANG II stimulated p38MAPK, but inhibited JNK; SB202190 inhibited both ANG II-induced podocyte apoptosis and p38MAPK phosphorylation; Inhibition of ERK by PD98059 had no effect on ANG II-induced cell apoptosis.