The antinociceptive effect of intrathecal escin in the rat formalin test

Antinociceptive effect of intrathecal amiloride on neuropathic pain in rats

“…In the uncontrolled activation of microglial cells under neuropathic pain conditions, the phosphorylated MAPK family induces the release of proinflammatory cytokines that facilitate pain transmission [18]. In the present study, intrathecal administration of 100 μg of amiloride was able to inhibit the expression of p-p38 MAPK and the activation of microglia in superficial laminae (I -II) of ipsilateral SDH and reduce pain-like behaviour, but no changes in contralateral SDH, consistent with the results of our previous study [15]. Amiloride can probably selectively block calcium channels to prevent Ca 2+ entry [23] and then inhibit the phosphorylation of p38.…”

“…Additionally, the pain behaviour was significantly reduced after intrathecal 100 μg of amiloride. Interestingly, our previous study showed that blocking formalin-induced hyperalgesia attenuated a formalin-induced increase of c-Fos in SDH [15]. These results are also consistent with previous experiments [20,31], indicating amiloride was able to suppress c-Fos expression in SDH neurons and further produce antinociception by inhibiting the activity of neurons.…”

“…In laminae I -II of L5 SDH, the number of Fos-immunoreactive (IR) was calculated under a microscope [15] and the area of p-p38-IR per section was measured using a computerized image analysis system (NIH ImagePro Plus 5.0, Media Cybernetics, Inc.) [8]. The mean ± SD were calculated for each treatment group.…”

“…Following the antinociception test, rats in both the 100-μg amiloride group and the control group were deeply anaesthetized with 10% chloral hydrate and perfused with 300 mL saline followed by 350 mL of 0.1 mol/L phosphate-buffered saline (PBS, pH 7.2-7.4, 4 °C) containing 4% paraformaldehyde for 30 min, as methods previously [8,15]. The L4 -L6 of spinal were removed, postfixed in 4% paraformaldehyde for 3 h, and then transferred to 30% sucrose for 2 days at 4 °C.…”

Pharmacokinetics of escin Ia in rats after intravenous administration

“…A number of reports have shown that escin exhibits remarkable antiinflammatory, antiedematous and vasoprotective properties and have been traditionally used to treat conditions such as chronic venous insufficiency (Greeske and Pohlmann, 1996;Ottillinger and Greeske, 2001;Pittler and Ernst, 2006), hemorrhoids (Guillaume and Padioleau, 1994), inflammation (Matsuda et al, 1997;Wei et al, 2004) and cerebral ischemic damage (Wetzel et al, 2002). In recent years, the pharmacological properties of escin have been studied extensively from different aspects, including sperm quality improvement, cerebral edema attenuation, liver protection, antitumor activity, and anti-allergic and anti-nociceptive effects (Fang et al, 2010;Jiang et al, 2011;Wang et al, 2011;Li et al, 2012;Sipos et al, 2012;Wang et al, 2012).…”