Progesterone Prevents Traumatic Brain Injury-Induced Intestinal Nuclear Factor kappa B Activation and Proinflammatory Cytokines Expression in Male Rats

نویسندگان

  • Gang Chen
  • Jinxin Shi
  • Yasuo Ding
  • Hongxia Yin
  • Chunhua Hang
چکیده

We have previously shown that traumatic brain injury (TBI) can induce an upregulation of nuclear factor kappa B (NF-kappaB) and proinflammatory cytokines in the gut, which play an important role in the pathogenesis of acute gut mucosal injury mediated by inflammation. In this work, we investigated whether progesterone administration modulated intestinal NF-kappaB activity and proinflammatory cytokines expression after TBI in male rats. As a result, we found that administration of progesterone following TBI could decrease NF-kappaB binding activity, NF-kappaB p65 protein expression, and concentrations of interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha) in the gut. TBI-induced damages of gut structure were ameliorated after progesterone injections. The results of the present study suggest that the therapeutic benefit of post-TBI progesterone injections might be due to its inhibitory effects on intestinal NF-kappaB activation and proinflammatory cytokines expression.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

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

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...

متن کامل

The Role of Proinflammatory Cytokines in Mediation of Brain Antiedema Effect of Female Sex Steroids Following Traumatic Brain Injury

Background & Aims: Release of proinflammatory cytokines after traumatic brain injury (TBI) is a major cause of brain edema. Previous studies demonstrated that sex steroids decrease brain edema induced by TBI. In this study changes of brain cytokines after the administration of estrogen and progesterone 24 hours after TBI were evaluated. Materials and Methods: Female rats were divided into 7 gro...

متن کامل

نقش محافظتی استروژن و پروژسترون بر بافت معدی به دنبال ایسکمی- رپرفیوژن معدی در موش‌های صحرایی نر

Background and Objective: Ischemia-reperfusion (I/R) injury repeatedly occurs in situations such as surgery, hemorrhage, burns, trauma, and infection. It has also been found that females were more resistant than males, indicating that female sex hormones have a protective function. The aim of this study was to determine the role of estrogen, progesterone, and their combination in protecting the...

متن کامل

Anti-Inflammatory Effects of Progesterone in Lipopolysaccharide-Stimulated BV-2 Microglia

Female sex is associated with improved outcome in experimental brain injury models, such as traumatic brain injury, ischemic stroke, and intracerebral hemorrhage. This implies female gonadal steroids may be neuroprotective. A mechanism for this may involve modulation of post-injury neuroinflammation. As the resident immunomodulatory cells in central nervous system, microglia are activated durin...

متن کامل

Ozone therapy could attenuate tubulointerstitial injury in adenine-induced CKD rats by mediating Nrf2 and NF-κB

Objective(s): This study aims to determine the effects of ozone therapy on restoring impaired Nrf2 activation to ameliorate chronic tubulointerstitial injury in rats with adenine-induced CKD. Materials and Methods: Sprague–Dawley rats were fed with 0.75% adenine-containing diet to induce CKD and chronic tubulointerstitial injury. Ozone therapy was administered by rectal insufflation. After 4 we...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Mediators of Inflammation

دوره 2007  شماره 

صفحات  -

تاریخ انتشار 2007