4 research outputs found

    Effect of Estrogen and Progesterone on Cytokines Levels at Different Time Intervals after Traumatic Brain Injury

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    Introduction: Following a traumatic brain injury (TBI), the excessive release of proinflammatory cytokines is major cause of cerebral edema that can cause permanent neuronal loss. This study examined the changes in brain concentrations of proinflammatory cytokines IL-1, IL-6, TNF-α and TGF- after different doses of estrogen or progesterone treatment in brain-injured rats at 6 and 24 h post-injury. Methods: Adult female rats were divided into 14 groups, and underwent either bilateral ovariectomy (12 groups) or sham surgery (2 groups). The hormones or vehicle were given intraperitoneally 0.5 h after TBI. Moderate TBI was induced by Marmarou method in TBI or treatment groups and brain levels of proinflammatory cytokines were measured 6 and 24 h post-injury. Results: The results indicated that high dose of estrogen (E2) and low dose of progesterone (P1) increase brain levels of IL-1 6 h post-injury by 52.8% and 79.2%, respectively compared to the vehicle. By the 24th h post-injury brain IL-1 level was reduced 27.5% and 27%, respectively compared to vehicle, when estrogen low dose (E1) and E2 were administered. Progesterone high dose treatment reduced brain level of IL-6 by 45.9% at 6 h post-injury and P1 treatment reduced IL-6 level by 20.5% at 24 h post-injury when compared to the vehicle. The brain TNF-α level was reduced by 72.5% by P2 at 6 h and 48.5% by E2 at 24 h post-injury, when compared to the vehicle. In addition, TGF- level seem to be increased by E1 up to 3.37 times at 24 h post-injury compared to the vehicle. Both doses of hormones showed increased levels of TGF- at 6 h post-injury, when compared to the vehicle. Conclusion: We conclude that progesterone and estrogen may change the levels of proinflammatory cytokines in the acute or delayed phases after TBI and this may be one of the mechanisms by which hormones reduce cerebral edema

    The Effects of Female Sex Steroids on Gastric Secretory Responses of Rat Following Traumatic Brain Injury

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    AbstractObjective(s)Gastric ulceration is induced by various forms of stress like surgery, ischemia and trauma. The female sex has more resistance to stress and the gastrointestinal lesions happen fewer than male sex. The purpose of this study was to evaluate the role of estradiol and progesterone on the gastric acid and pepsin levels following traumatic brain injury (TBI) induction.Materials and MethodsDiffuse TBI was induced by Marmarou method in female rats. Rats randomly assigned into 9 groups: intact, OVX (ovarectomized rat), Sham+OVX, TBI (intact rats under TBI), TBI+OVX (ovarectomized rats under TBI) and treated OVX rats with vehicle (sesame oil), E2 (estradiol), P4 (progesterone) or E2+P4 combination. The acid content and pepsin levels of each gastric washout sample were measured 5 days after the TBI induction.ResultsThere was no significant difference in gastric acid output between groups either after TBI induction or after treatment with E2 or P4 or E2+P4. Gastric pepsin levels were increased in Sham+OVX, TBI (P< 0.001) and TBI+OVX (P< 0.05) compared to intact group. Gastric pepsin levels were significantly lower in E2 and E2+ P4 treated rats than vehicle treated group (P< 0.01). P4 treatment increased gastric pepsin level compared to TBI+OVX group (P< 0.05) and this increment was higher than rats that were treated with the E2 and E2+P4 (P< 0.01).ConclusionThese results suggest that protective effect of estradiol and E2+P4 combination against mucosal damage after TBI, might be mediated by inhibition of pepsin secretion

    Short Communication Effect of trifluoperazine on carrageenan-induced acute inflammation in intact and adrenalectomized rats

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    Abstract: The aim of present study was to investigate the effect of trifluoperazine (TFP) on carrageenaninduced rat&apos;s paw edema in intact and adrenalectomized (ADX). TFP (0.2 and 8 mg/kg) were given intraperitoneally just before the intraplantar injection of 0.1 ml of 0.5% carrageenan solution. After four hours, paw edema was assessed by calculating the paw volume changes and extravasations of Evans blue dye as inflammatory indicators. In both ADX and control groups, administration of TFP reduced inflammatory parameters (paw volume and tissue content of Evans blue dye) in inflamed paw. Our findings suggest that TFP can effectively reduce carrageenan-induced paw edema in both ADX and control rats. Therefore, antiinflammatory effect of these drugs does not need the adrenal gland activity
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