The Inflammation in the Gut After Experimental Subarachnoid Hemorrhage

Zhou, Meifang; Zhu, Lin; Wang, Jian; Hang, Chun-Hua; Shi, Jinjie

doi:10.1016/j.jss.2006.06.023

Cited by 26 publications

(21 citation statements)

References 30 publications

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“…Besides those complications, gastrointestinal dysfunction could be frequently observed in the patients suffering from SAH [10]. Gastrointestinal dysfunction may initiate a cascade of intestinal events such as intestinal cytokine overproduction, increased intestinal permeability and translocation of intestinal bacteria and endotoxins [11,12]. These events may not only influence the intestinal mucosa itself, but also may affect the function and integrity of remote organs and tissues, leading to systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) [13].…”

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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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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“…Some of the possible mechanisms underlying the activity of these hormones against ulcerative effects of traumatic brain injuries are: maintaining calcitonin gene relevant peptide (CGRP) level, that has the protective role in mucosal injuries [96], over-production of mucosal secretion by gastric mucosal [17], the increase of bicarbonate secretion from gastric mucosal like to the increased secretion of bicarbonate from duodenum mucosal by estrogen [47], alteration of hypothalamic pituitary axis (HPA) is response to stress [86], the reduction of vascular epidermal growth factor (VEGF) secretion in stomach [97], inhibition of oxidative stress [98], modulation of nitric oxide (NO) production [99], regulation of autonomic nervous system activity [100], interaction with melatonin in gastric mucosal level [101], promotion of angiogenesis [102], reduction of gastric inflammation by decreasing TNF-α release [103], and inhibition of apoptosis due to ischemia [104].…”

Section: Tbi Gi Tract and Sex Hormonesmentioning

confidence: 99%

Traumatic Brain Injury and the Gastrointestinal Tract: The Role of Female Sexual Hormones

et al. 2017

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Traumatic brain injury (TBI) is an important public health problem which can lead to several complications like gastrointestinal dysfunction. Patients with TBI often suffer from gastrointestinal dysfunctions such as enteral feeding intolerance. Gastric ulceration is induced by various forms of stress like surgery, ischemia and trauma. TBI causes a delayed but significant decrease in intestinal contractile activity in the ileum leading to delayed transport. The association between severity of brain injury and enteral feeding intolerance suggests a strong link between the central nervous system and the non-functional gut. The results of recent basic and clinical studies revealed the beneficial effects of estrogen and progesterone hormones in the treatment of gastrointestinal dysfunction. Females have more resistance to stress and fewer gastrointestinal lesions occur in females as compared to males. Sex steroid hormones have sparked interest as possible neuroprotective agents after traumatic injury and many studies have been done on this subject. This article reviews the literature related to some possible physiological effects of female sexual hormones on the gastrointestinal tract following TBI.

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“…Nuclear protein was extracted and quantified as described by Zhou ML, et al [26]. Briefly, frozen brain samples were homogenized in 0.8 ml ice-cold buffer A composed of 10 mmol/l HEPES pH 7.9, 10 mmol/l KCl, 2 mmol/l MgCl 2 , 0.1 mmol/l EDTA, 1 mmol/l dithiothreitol (DTT), and 0.5 mmol/l phenylmethylsulfonyl fluoride (PMSF) (all from Sigma Chemical Co., St. Louis, Mo, USA).…”

Section: Nuclear Protein Extract and Emsa For Nf-jbmentioning

confidence: 99%

“…EMSA was performed using a commercial kit (Gel Shift Assay System; Promega, Madison, Wis, USA) following the methods in our laboratory [26]. Consensus oligonucleotide probe (5-AGTTGAGGGGACTTTCCCAGGC-3) was endlabeled with [c-32P] ATP (Free Biotech., Beijing, China) with T4-polynucleotide kinase.…”

Section: Nuclear Protein Extract and Emsa For Nf-jbmentioning

confidence: 99%

Hydrogen-Rich Saline is Cerebroprotective in a Rat Model of Deep Hypothermic Circulatory Arrest

et al. 2011

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Deep hypothermic circulatory arrest (DHCA) has been widely used in the operations involving the aortic arch and brain aneurysm since 1950s; but prolonged DHCA contributes significantly to neurological deficit which remains a major cause of postoperative morbidity and mortality. It has been reported that hydrogen exerts a therapeutic antioxidant activity by selectively reducing hydroxyl radical. In this study, DHCA treated rats developed a significant oxidative stress, inflammatory reaction and apoptosis. The administration of HRS resulted in a significant decrease in the brain injury, together with lower production of IL-1β, TNF-α, 8-OHdG and MDA as well as decreased activity of NOS while increased activity of SOD. The apoptotic index as well as the expressions of caspase-3 in brain tissue was significantly decreased after treatment. HRS administration significantly attenuated the severity of DHCA induced brain injury by mechanisms involving amelioration of oxidative stress, down-regulation of inflammatory factors and reduction of apoptosis.

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The Inflammation in the Gut After Experimental Subarachnoid Hemorrhage

Cited by 26 publications

References 30 publications

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

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

Traumatic Brain Injury and the Gastrointestinal Tract: The Role of Female Sexual Hormones

Hydrogen-Rich Saline is Cerebroprotective in a Rat Model of Deep Hypothermic Circulatory Arrest

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