1.广州中医药大学基础医学院 广东 510006
2.福建中医药大学附属第二人民医院
李思汉,男,在读博士生
# 通信作者:黄铭涵,男,硕士,副主任医师,硕士生导师,主要研究方向:慢性萎缩性胃炎的临床与基础研究,E-mail:huangminghan2010@163.com
收稿:2020-08-20,
纸质出版:2021-02-28
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李思汉, 林秀明, 田琳, 等. 健脾清化舒络中药对慢性萎缩性胃炎大鼠Sonic Hedgehog信号通路的影响[J]. 北京中医药大学学报, 2021,44(2):143-151.
Sihan Li, Xiuming Lin, Lin Tian, et al. Effect of spleen-fortifying, fire-clearing and collateral-unblocking medicinals on Sonic Hedgehog signaling pathway in rats with chronic atrophic gastritis[J]. Journal of Beijing University of traditional Chinese Medicine, 2021, 44(2): 143-151.
李思汉, 林秀明, 田琳, 等. 健脾清化舒络中药对慢性萎缩性胃炎大鼠Sonic Hedgehog信号通路的影响[J]. 北京中医药大学学报, 2021,44(2):143-151. DOI: 10.3969/j.issn.1006-2157.2021.02.009.
Sihan Li, Xiuming Lin, Lin Tian, et al. Effect of spleen-fortifying, fire-clearing and collateral-unblocking medicinals on Sonic Hedgehog signaling pathway in rats with chronic atrophic gastritis[J]. Journal of Beijing University of traditional Chinese Medicine, 2021, 44(2): 143-151. DOI: 10.3969/j.issn.1006-2157.2021.02.009.
目的
2
探讨健脾清化舒络中药对慢性萎缩性胃炎(CAG)大鼠Sonic Hedgehog信号通路的影响。
方法
2
雄性Wistar大鼠59只,随机分为空白对照组16只、造模组43只,采用复合造模法进行病证结合CAG模型构建,期间随机抽取造模组大鼠3只验证CAG造模是否成功。造模成功后,予健脾清化舒络中药(复方胃炎合剂)进行相关干预。具体干预方案为:将空白对照组随机分为空白组、健脾清化舒络中药高剂量[61.04 g/(kg·d)]空白组,造模组随机分为CAG模型组、维酶素[0.2 g/(kg·d)]组和健脾清化舒络中药低、中、高剂量[15.26、30.52、61.04 g/(kg·d)]组,每组8只,给予相应药物连续干预4周。检测大鼠胃组织Shh、Ptch1、Smo、Gli1、Gli2、Gli3、Sufu蛋白表达水平及血清中白细胞介素-1β(IL-1β)、胃泌素(GAS)含量。
结果
2
与空白组比较,模型组大鼠Shh、Ptch1、Smo、Gli1蛋白表达及血清GAS水平降低,Gli2、Gli3、Sufu蛋白表达及血清IL-1β水平上升,差异均有统计学意义(
P
<
0.05、
P
<
0.01)。与CAG模型组比较,健脾清化舒络中药低、中、高剂量组胃黏膜病变显著改善,Shh、Ptch1、Smo、Gli1蛋白表达上调,Gli2、Gli3、Sufu蛋白表达下调,血清IL-1β水平降低,差异均有统计学意义(
P
<
0.05、
P
<
0.01),健脾清化舒络中药中、高剂量组血清GAS水平上升(
P
<
0.05)。
结论
2
健脾清化舒络中药可有效改善CAG大鼠胃黏膜组织病理改变,其机制可能与调控血清IL-1β、GAS含量,重新激活下游Sonic Hedgehog信号通路的表达有关。
Objective
2
To explore the effect of spleen-fortifying
fire-clearing and collateral-unblocking (SFC) medicinals on Sonic Hedgehog signal pathway in rats with chronic atrophic gastritis (CAG).
Methods
2
59 male wistar rats were randomly divided into the control group (
n
= 16) and model group (
n
= 43). The CAG model was established by comprehensive modeling method. After that
3 rats in the model group were randomly selected for gastric pathological examination. After the model was successfully established
the compound gastritis mixture (under the guidance of the SFC method) was given as a representative drug for relevant intervention. Specifically
the control group was randomly divided into blank group
blank + high dose SFC group
while the model group was randomly divided into CAG group
Vitacoenzyme group
low dose
medium dose and high dose SFC groups (n=8). The corresponding drugs were given continuously for 4 weeks. At last
the protein expression levels of Shh
Ptch1
Smo
Gli1
Gli2
Gli3 and Sufu in gastric tissue and the concentration of IL-1 β and GAS in serum were measured.
Results
2
In the model group
the expression of Shh
Ptch1
Smo
Gli1 protein and the level of serum GAS decreased
while the expression of Gli2
Gli3
Sufu protein and the level of serum IL-1β increased (
P
<
0.05
P
<
0.01). Compared with the CAG group
the pathological changes of gastric mucosa in the low
middle and high dose SFC groups were significantly improved
the expression of Shh
Ptch1
Smo and Gli1 protein increased
and the expression of Gli2
Gli3
Sufu protein and the level of serum IL-1β decreased (
P
<
0.05
P
<
0.01). The level of serum GAS in middle and high dose SFC groups increased significantly (
P
<
0.05).
Conclusion
2
SFC method could possibly improve the pathological changes of CAG in rats
and its mechanism may be related to improving the contents of serum IL-1β and GAS and reactivating the expression of Sonic Hedgehog signal pathway.
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