Alleviation of neuropathic pain by regulating T-type calcium channels in rat anterior cingulate cortex.

BACKGROUND: It has been demonstrated that administration of T-type calcium channel (TCC) inhibitors could relieve the neuropathic pain by intraperitoneally or intrathecally. TCCs are not only expressed in dorsal root ganglia or dorsal horn, but also in some of the pain associated brain regions. In the present study, we sought to investigate whether modulating TCCs in the anterior cingulate cortex (ACC) could alleviate the neuropathic pain. RESULTS: (1) Cav3.2 was up regulated in rat ACC after chronic constriction injury (CCI). (2) T-type calcium current intensity was increased in CCI animal model. (3) TCC inhibitor reduced miniature excitatory postsynaptic currents frequency of ACC neurons in CCI animal model. (4) TCC inhibitor suppressed the firing rate of ACC neurons in CCI animal model. (5) Both mechanical and thermal allodynia were partially relieved by ACC microinjection with TCC inhibitor. CONCLUSIONS: TCCs in the ACC may be contributing to the maintenance of neuropathic pain, and the neuropathic pain can be alleviated by inhibiting the neuronal activity of ACC through modulating the TCCs.

Diosgenin attenuates hepatic stellate cell activation through transforming growth factor-ß/Smad signaling pathway.

Activation of hepatic stellate cells (HSC) plays a pivotal role in the development of hepatic fibrosis. Transforming growth factor-ß1 (TGF-ß1) is considered to be the main stimuli factor responsible for the activation of HSC. Diosgenin is a steroidal saponin found in several plants including Solanum and Dioscorea species, and it inhibited high glucose-induced renal tubular fibrosis. However, the effects of diosgenin against hepatic fibrosis remain elusive. Therefore, in this study, we investigated the effects of diosgenin on TGF-ß1-induced HSCs and elucidate the possible mechanism of its anti-fibrotic effect. Our results demonstrated that diosgenin inhibited TGF-ß1-induced HSC proliferation, reduced the expression of collagen I and α-smooth muscle actin (α-SMA), as well as the expression of TGF-ß receptor I (TGF-ß RI) and II. Moreover, diosgenin suppressed TGF-ß1-induced phosphorylation of Smad3 in HSCs. In conclusion, our data demonstrate that diosgenin inhibited HSC-T6 cell proliferation and activation, at least in part, via the TGF-ß1/Smad signaling pathway. These results provide that diosgenin may have potential to treat liver fibrosis.

The risk factors for nosocomial infection in chinese patients with active rheumatoid arthritis in shanghai.

Objective. To analyse the potential risk factors of nosocomial infections in patients with active rheumatoid arthritis (RA). Methods. A total of 2452 active RA patients at Hospitals in Shanghai between January 2009 and February 2011 were analyzed. Their demographic and clinical characteristics were compared with those without infection, and the potential risk factors were determined by logistic regression analysis. Results. Multivariate analysis indicated the gender (OR = 0.70, 95% CI 0.53-0.92), duration in hospital (OR = 1.03 , 95%CI 1.01-1.05), number of organs involved (OR = 0.82, 95%CI 0.72-0.92), number of disease-modifying antirheumatic drugs ((DMARDs) (OR = 1.22, 95%CI 1.061-1.40)), corticosteroid therapy (OR = 1.02, 95%CI 1.01-1.03), peripheral white blood cell counts ((WBC) (OR = 1.04, 95%CI 1.00-1.08)), levels of serum albumin (OR = 0.98, 95%CI 0.97-0.99), and C-reactive protein ((CRP) (OR = 1.03 , 95%CI 1.01-1.04)) that were significantly associated with the risk of infections. Conclusion. The female patients, longer hospital stay, more organs involved, more DMARDs, corticosteroid usage, high counts of WBC, lower serum albumin, and higher serum CRP were independent risk factors of infections in active RA patients.