氫水還原健康-氫氣治療小腸移植後炎症損傷

 

總體印象,美國對氫在器官移植方面非常關注,在心臟和小腸方面都已經開始出文章了。我們必須加緊這方面的工作,否則就要落後了。

該論文在實驗技術上沒有新東西,採用HE、小腸黏膜通透性、小腸體外張力功能測定,並用定量 PCR測定了幾個重要炎症分子的 mRNA。實驗非常簡單。

但該文章寫的比較好,基本把目前氫有關的研究都包括進,而且把 2001年最早的一個法國的報導也用上了。儘管我早就注意到這個,但我們論文中沒有引用,是我們的不足,值得學習。

該文比較可貴的是測定了動脈血中的氫濃度,呼吸後比正常升高了 3.5倍。這個文章強調了體內細菌產生氫的量比較可觀,比日本的文章要有進步。我曾經與日本學者討論這個問題,他們說測不出來。現在的結果更明確了。

另外這個資料說明,呼吸氫並沒有十分明顯增加氫的量,更說明氫的作用重要,同時也提示內源性氫可能具有重要作用。文章在這個問題上提出,大腸對缺血與小腸相比不敏感,主要可能是大腸有細菌,可產生氫。內氫的作用值得我們重視。

該文在討論中談到, HO-1IL-10可以升高,而這些物質是抗氧化和抗炎症的。因此可以作為將來我們研究的測定指標。

在討論中,作者認為線粒體通透性可能受到影響,可作為將來的一個指標進行研究。當然細胞凋亡相關的蛋白都是可以的。細胞的研究,很多信號分子都可以進行研究和探索。

本研究只是用 PCR測定,沒有用蛋白和酶學方法,是非常遺憾的,也是我們可以考慮在其基礎上改進提高的。

Molecular hydrogen prevents intestinal I/R injury

Takeshi Tsukamoto MD , Bettina M. Buchholz MD , Asad Nazir MD , R. Savanh Chanthaphavong PhD , Christopher Pape MD , Atsunori Nakao MD and Anthony J. Bauer PhD a

 

University of Pittsburgh, Pittsburgh, PA

Available online 27 August 2008. 

 

Article Outline

Introduction
Methods
Results
Conclusions

 

 

 

Introduction

 

Molecular hydrogen shows potential for reducing ischemia/reperfusion (IR) injury. We investigate the effect of hydrogen on intestinal IR injury.

 

 

Methods

 

Rodents were subjected to SMA clamp IR (50min) and reperfusion with air or molecular hydrogen (2%) inhalation (30 pretreatment/50min ischemia/30min posttreatment). Histochemistry and IHC on jejunal muscularis whole-mounts quantified neutrophil and F4/80+ monocyte recruitment into the muscularis externa (N=4 each). Organ bath recordings measured jejunal circular muscle contractility to bethanechol (0.3-300μM, N=6 each). Orally fed FITC-fluorescent microspheres (0.4μM) within muscularis leukocytes assessed mucosal barrier function .

 

Results

 

Few neutrophils were observe in air and hydrogen treated controls (Air=1.1±0.23 vs. Hydrogen=0.6±0.14). I/R resulted in a significant increase in neutrophils into the muscularis of air treated mice (46.2±8.19), which was significantly decreased by hydrogen inhalation (16.7±4.69). Monocytes were not observed within control tissues, but I/R air mice exhibited the appearance of dense monocytic plaques at 24 hours. Hydrogen treated animals did not exhibit the monocytic plaques. Bethanechol dose-response curves demonstrated no difference between air and hydrogen treated control mice or 3hrs after reperfusion. However, 24 hours after reperfusion hydrogen treatment resulted in markedly improved muscle contractility compared to air (Air-I50min/R24hrs=0.26±0.071 vs. Hydrogen-I50min/R24hrs =0.68±0.118 g/mm2/sec @ 100μM bethanechol). I/R resulted in a time dependent lumeno-lymphatic transference of microspheres in 30 minutes after reperfusion that was blocked by lymphatic ligation.

 

Conclusions

 

I/R injury causes a breakdown in mucosal barrier function, neutrophil and monocyte recruitment into the muscularis externa resulting in a suppression in muscle function, which is significantly prevented by molecular hydrogen.

全文

 

 


 

  

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