ERKl/2 signaling pathway mediates heme oxygenase-1 up-regulation by minocycline in PC12 cells exposed to oxygen glucose deprivation / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effects of minocycline in promoting the survival of pheochromocytoma (PCI2) cells exposed to oxygen glucose deprivation (OGD) and explore the underlying mechanisms.</p><p><b>METHODS</b>An in vitro cell model of cerebral ischemia was established by OGD for 6 h in PCI2 cells with pretreatment with minocycline or an ERK1/2 inhibitor. At 24 h after OGD injury, the cells were evaluated for cell viability by MTT assay and expressions of heme oxygenase-I (HO-I) and phospholylated extracellular signal-regulated protein kinase 1/2 (ERK1/2) by Western blotting.</p><p><b>RESULTS</b>The cell viability decreased dramatically following OGD. Pretreatment with minocycline (O.I-IO JJ.mol/L) induced a significant increase in the cell viability after OGD and caused up-regulation of HO-I protein and enhanced ERK1/2 phospholylation, and the effects were especially obvious with 1 JJ.mol/L minocycline and were abolished by inhibition of ERK1/2 activity with UOI26 (IO JJ.mol/L).</p><p><b>CONCLUSION</b>Minocycline can protect PCI2 cells against OGD-induced toxicity by up-regulating HO-I protein expression through ERKl/2 signaling pathways.</p>

Neuroelectrophysiological characteristics of Hirayama disease: report of 14 cases / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hirayama disease is a juvenile muscular atrophy of the distal upper extremities and affects mainly young males. The present study aimed to investigate the neuroelectrophysiological characteristics of Hirayama disease.</p><p><b>METHODS</b>We retrospectively analyzed the neural conduction velocity (NCV) parameters and needle-electrode electromyograms (EMG) of 14 patients with Hirayama disease. According to the clinical features of the patients, NCV was performed on affected upper-limb including median nerves and ulnar nerves, while EMG was selectively performed on upper and lower extremities, sternocleidomast and thoracic paraspinal muscles.</p><p><b>RESULTS</b>The median nerves of all affected upper limbs of patients with Hirayama disease had normal conduction velocities and compound motor action potentials (CMAPs). The ulnar nerves of all affected upper limbs also had normal conduction velocities. Of the 16 measured ulnar nerves of the affected upper limbs, eight had normal CMAPS, while the other eight showed CMAPs below the normal value by < 20%. All patients had neurogenic injury on the affected side in muscles innervated by anterior horn cells at the lower cervical region (C7-8, T1). Four patients had unilateral upper-limb muscle neurogenic injury on the affected side. Seven patients had bilateral upper-limb muscle neurogenic injury, while only two patients experienced bilateral upper-limb muscle atrophy/weakness. The other three patients showed extensive neurogenic injury (unilateral upper-limb muscle atrophy/weakness in one patient, bilateral symptoms in the other two patients).</p><p><b>CONCLUSIONS</b>Electromyographic examination showed that the majority of Hirayama disease patients exhibited characteristic segmental injury in the anterior horn of the lower cervical region, while a few patients exhibited extensive neurogenic injury. These data suggest that the actual influence of Hirayama disease may be more extensive than indicated by the clinical presentations.</p>

Effects of carbon disulfide on the expression and activity of nitric oxide synthase in rat hippocampus / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Carbon disulfide (CS(2)) is a commonly used organic solvent. Many epidemiological investigations and animal experiments have indicated that learning and memory ability can be affected to different degrees after long-term exposure to CS(2), but the mechanisms are still unclear. The aim of this study was to explore the possible mechanisms of CS(2)-related impairment of the learning and memory ability of rats, by investigating the effects of CS(2) on nitric oxide synthase (NOS) activity and NOS mRNA expression in rat hippocampus.</p><p><b>METHODS</b>Rat models of toxicity were generated by inhalation of various doses of CS(2). After two months of inhaling intoxication, the activities of constitutive NOS (cNOS) and induced NOS (iNOS) in the hippocampus were measured. The levels of neuronal NOS (nNOS) mRNA and iNOS mRNA were measured by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>cNOS activity was significantly decreased compared with controls, while iNOS activity was changed only slightly. CS(2) treatment significantly decreased nNOS mRNA levels. iNOS mRNA levels were significantly increased only at higher doses of CS(2).</p><p><b>CONCLUSION</b>The effect of CS2 on learning and memory ability in rats is related to the activity of NOS and the expression of nNOS in the hippocampus.</p>