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药学翻译-硫化氢与细胞信号通路

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药学翻译-硫化氢与细胞信号通路 本文关键词:硫化氢,通路,药学,细胞,信号

药学翻译-硫化氢与细胞信号通路 本文简介:药学翻译-硫化氢与细胞信号通路泛瑞翻译作者:LiL,RoseP,MoorePK.AnnuRevPharmacolToxicol.2011;51:169-87.PMID:21210746摘要硫化氢(H2S)是胱硫醚γ-裂解酶(CSE)与其他自发酶类分解半胱氨酸所得的一种气体递质。H2S供体药理学试验与

药学翻译-硫化氢与细胞信号通路 本文内容:

药学翻译-硫化氢与细胞信号通路

泛瑞翻译

作者:Li

L,Rose

P,Moore

PK.

Annu

Rev

Pharmacol

Toxicol.

2011;

51:169-87.

PMID:

21210746

摘要

硫化氢(H2S)是胱硫醚γ-裂解酶(CSE)与其他自发酶类分解半胱氨酸所得的一种气体递质。H2S供体药理学试验与CSE基因敲除小鼠遗传实验表明该血管扩张性气体在血管直径、局部缺血/再灌注损伤心脏应变与炎症调节方面有重要作用。几十年前,已确认H2S可抑制细胞色素c氧化酶,并可降低细胞内能量产生。但近年来,发现该气体存在大量其他的药理学靶标。H2S可激活KATP与瞬时受体电位(TRP)通道,常抑制大电导钙激活钾(BKCa)通道、T型钙通道与M型钙通道。H2S可抑制或激活NF-κB核转运,并影响大量激酶的活性,如p38丝裂原活化蛋白激酶(p38

MAPK)、细胞外信号调节激酶(ERK)与Akt等。这些不同效应可能继发于H2S已知的还原性和/或促进细胞内蛋白质半胱氨酸氢硫化的性质。

原文:

Title:

Hydrogen

Sulfide

and

Cell

Signaling

Author:

Li

L,Rose

P,Moore

PK.

Annu

Rev

Pharmacol

Toxicol.

2011;

51:169-87.

PMID:

21210746

Abstract

Hydrogen

sulfide

(H2S)

is

a

gaseous

mediator

synthesized

from

cysteine

by

cystathionine

γ

lyase

(CSE)

and

other

naturally

occurring

enzymes.

Pharmacological

experiments

using

H2S

donors

and

genetic

experiments

using

CSE

knockout

mice

suggest

important

roles

for

this

vasodilator

gas

in

the

regulation

of

blood

vessel

caliber,cardiac

response

to

ischemia/reperfusion

injury,and

inflammation.

That

H2S

inhibits

cytochrome

c

oxidase

and

reduces

cell

energy

production

has

been

known

for

many

decades,but

more

recently,a

number

of

additional

pharmacological

targets

for

this

gas

have

been

identified.

H2S

activates

KATP

and

transient

receptor

potential

(TRP)

channels

but

usually

inhibits

big

conductance

Ca2+-sensitive

K+

(BKCa)

channels,T-type

calcium

channels,and

M-type

calcium

channels.

H2S

may

inhibit

or

activate

NF-κB

nuclear

translocation

while

affecting

the

activity

of

numerous

kinases

including

p38

mitogen-activated

protein

kinase

(p38

MAPK),extracellular

signal-regulated

kinase

(ERK),and

Akt.

These

disparate

effects

may

be

secondary

to

the

well-known

reducing

activity

of

H2S

and/or

its

ability

to

promote

sulfhydration

of

protein

cysteine

moieties

within

the

cell.

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