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

Chen, Gang; Shi, Jinxin; Ding, Yasuo; Yin, Hong-Xia; Hang, Chun-Hua

doi:10.1155/2007/93431

Cited by 40 publications

(39 citation statements)

References 32 publications

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“…Protective effects of progesterone in the acutely injured brain include decreased neuroinflammation and secondary injury through multiple pathways, including NFκB and mitogen-active protein kinases [40,41,42,43]. Further, progesterone decreases reactive oxygen species through its effects on mitochondria in multiple tissue types, including the brain [43,44].…”

Section: Discussionmentioning

confidence: 99%

Progesterone Improves Neurobehavioral Outcome in Models of Intracerebral Hemorrhage

Lei

Wang²,

Jeong³

et al. 2015

Neuroendocrinology

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In models of acute brain injury, progesterone improves recovery through several mechanisms including modulation of neuroinflammation. Secondary injury from neuroinflammation is a potential therapeutic target after intracerebral hemorrhage (ICH). For potential translation of progesterone as a clinical acute ICH therapeutic, the present study sought to define efficacy of exogenous progesterone administration in ICH-relevant experimental paradigms. Young and aged C57BL/6 male, female, and ovariectomized (OVX) mice underwent left intrastriatal collagenase (0.05-0.075 U) or autologous whole blood (35 μl) injection. Progesterone at varying doses (4-16 mg/kg) was administered at 2, 5, 24, 48, and 72 h after injury. Rotarod and Morris water maze latencies were measured on days 1-7 and days 28-31 after injury, respectively. Hematoma volume, brain water content (cerebral edema), complementary immunohistochemistry, multiplex cytokine arrays, and inflammatory proteins were assessed at prespecified time points after injury. Progesterone (4 mg/kg) administration improved rotarod and water maze latencies (p < 0.01), and decreased cerebral edema (p < 0.05), microglial proliferation, and neuronal loss (p < 0.01) in young and aged male, young OVX, and aged female mice. Brain concentration of proinflammatory cytokines and Toll-like receptor-associated proteins were also decreased after progesterone (4 mg/kg) treatment (p < 0.01). Progesterone-treated young female mice showed no detectable effects. Exogenous progesterone improved short- and long-term neurobehavioral recovery and modulated neuroinflammation in male and OVX mice after ICH. Future studies should validate these findings, and address timing and length of administration before translation to clinical trial.

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Section: Discussionmentioning

confidence: 99%

Progesterone Improves Neurobehavioral Outcome in Models of Intracerebral Hemorrhage

Lei

Wang²,

Jeong³

et al. 2015

Neuroendocrinology

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“…intestinal mucosal structure [17,18]. However, until now no study was found in the literature to investigate the effects of progesterone on intestinal inflammatory response and mucosa structure alterations after SAH.…”

Section: Introductionmentioning

confidence: 99%

Effects of Progesterone on Intestinal Inflammatory Response and Mucosa Structure Alterations Following SAH in Male Rats

Zhao

Zhou

2011

Journal of Surgical Research

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“…Our research provided direct evidence that nongenomic effect of progesterone could restrain iNOS activation mediated by P38MAPK signal pathway. This effect resulted in a decrease in serum NO concentration in infectious women, caused anti-inflammation, and played a certain role in asymptomatic infections [26] . Although nongenomic effect of progesterone in asymptomatic infections is limited, it can provide a piece of clue to elucidate the phenomenon.…”

Section: Discussionmentioning

confidence: 99%

The nongenomic effects of progesterone in repressing iNOS activation through P38MAPK pathways in gonococci-infected polymorphonuclear leukocytes and the clinical significance

Chen

Lin

et al. 2010

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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Progesterone has nongenomic effects on inducible nitric oxide synthase (iNOS), which is mediated by mitogen activated protein kinase (MAPK) pathways. This effect is supposed to have some potential association with asymptomatic gonococcal infections in women by immunological depression. In this study, polymorphonuclear leukocytes (PMNs) challenged by gonococci were used to study the nongenomic effects of progesterone. The activation of iNOS was assessed by measuring [(3)H] L-arginine converses to [(3)H] L-citrulline, and the activity of MAPK was detected by Western blot. It was found that the activity of iNOS and the yields of NO were enhanced significantly in gonococci-challenged PMNs compared with the controls (P<0.01). Progesterone could repress the activation of iNOS through P38MAPK pathway within PMNs (P<0.05), which could be blocked by SB203580 (P<0.01), but not by actinomycin D (P>0.05). It was also found subsequently that in the serum specimens collected from gonococci-infected but asymptomatic women, the progesterone level was higher than that in women with severe symptoms (P<0.01). Moreover, the yield of NO had an inverse correlation with progesterone. With these results it suggested that the rapid nongenomic effects of progesterone may inhibit iNOS activation and NO yields mediated by P38MAPK pathways, which were supposed to be concerned with asymptomatic women infected with gonococci.

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

Cited by 40 publications

References 32 publications

Progesterone Improves Neurobehavioral Outcome in Models of Intracerebral Hemorrhage

Progesterone Improves Neurobehavioral Outcome in Models of Intracerebral Hemorrhage

Effects of Progesterone on Intestinal Inflammatory Response and Mucosa Structure Alterations Following SAH in Male Rats

The nongenomic effects of progesterone in repressing iNOS activation through P38MAPK pathways in gonococci-infected polymorphonuclear leukocytes and the clinical significance

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