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MessagePosté le: Mar 1 Juil - 07:06 (2014) Sujet du message: Since the immune related pathways have the most direct rele Répondre en citant

 0 saline were pre treated with a potent P2X antagonist, TNP ATP or a selective buy AP24534 P2Y1 antagonist, MRS2179. Animals were pretreated with TNP ATP or MRS2179 daily 30 min before the 4. 0 saline injec tion. MRS2179 dose dependently blocked the develop ment of TH, while TNP ATP did not affect the onset of TH. Peripheral P2Y1 receptors modulate TRPV1 activity by PKC dependent phosphorylation in acidic saline injected TIIP rats Since P2Y1 receptors appeared to play a crucial role in acidic saline induced TH in TIIP rats, an additional experiment was performed to test the hypoth esis that P2Y1 receptors might modulate TRPV1 activity under ischemic conditions. To address this, we performed a western blot analysis of phosphorylated TRPV1 in the hind paw skin of sham vehicle, AS TIIP vehicle and AS TIIP MRS2179 groups at postoperative day 3 following daily injections of pH 4.

0 saline. Vehicle and MRS2179 were repetitively injected into the hind paw 30 min before pH 4. 0 saline in jection. Acidic saline injection into the hind paw of TIIP rats increased the expression of pTRPV1. More importantly, repeated i. pl treatment with MRS2179 prior to the pH 4. 0 saline AT7519 844442-38-2 injection returned the expression of pTRPV1 to baseline levels. Quantitative analysis of pTRPV1 expression was normalized against corresponding total TRPV1 expression and calculated as a percent change with respect to the sham group. Discussion It has been reported that tissue acidity corresponds to the severity of hypoxic status, and the tissue acidic envir onment is a major factor for triggering ischemia related pathological consequences.

In terms of pain hypersensitivity, although low tissue pH at the ischemic site has been considered a crucial factor in the develop ment of ischemic pain, the contribution of the acidic environment to ischemia induced FDA approved Akt 阻害剤 thermal hyper sensitivity has not been delineated. The present study is the first to demonstrate that under peripheral ischemic conditions an increase in tissue acidity results in the de velopment of thermal hyperalgesia. Here, we injected pH 4. 0 saline into the ischemic hind paw to evaluate how an acidic tissue environment affected both thermal hyper sensitivity and TRPV1 activity under peripheral ischemic condition.

Since hypoxia inducible factor 1α is a well known indicator of hypoxia and carbonic anhydrase II has been reported to be a major indicator of pH imbalance, we examine changes in these two fac tors in order to evaluate the degree of hypoxic injury and tissue acidity. We observed that repetitive acidic saline in jection into the ischemic hind paw increased protein levels of both hypoxia inducible factor 1α and carbonic anhydrase II in hind paw muscle. These results indicated that the presence of an acidic tissue envir onment intensified the ischemia associated insults to the hind paw muscle tissue. Therefore, we postulate that injec tion of acidic saline into TIIP rats represents a model of the ischemic condition with severe tissue acidosis. Since the injection of pH 4. 0 saline solution itself in sham rats did not affect thermal nociception, these findings indicated that an increased acidic environ ment in the presence of other pro algesic substances under ischemic conditions could lead to the development of TH.

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MessagePosté le: Mar 1 Juil - 07:06 (2014) Sujet du message: Publicité

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