Objective To explore the possible mechanism of Yangyin Tongnao Keli（ 养阴通脑颗粒） decreasing cerebral ischemia reperfusion injury. Methods Totally 162 Sprague Dawley（ SD） rats were randomized into sham operation group

model group and Yangyin Tongnao Keli group

with 54 rats in each group. The model group and the Yangyin Tongnao Keli group were established cerebral ischemia reperfusion injury models by middle cerebral artery focal embolism operation. The Yangyin Tongnao Keli group was given Yangyin Tongnao Keli 0. 5 g/kg by gavage every12 hours. The sham operation group and the model group were given equivalent normal saline. After 12

24

48

and72 hours of modeling

neurological deficit score

glucose regulated protein 78（ GRP78） in CA1 area of hippocampus

protein kinase R-like ER kinase（ PERK） and the expressions of mRNA

as well as the mRNA expressions of eukaryotic translation initiation factor 2α（ e IF2α）

endoplasmic reticulum derived transcription factor CCAAT/enhancer binding protein homologous protein（ chop） and activating transcription factor 4（ ATF4） were observed. The volume of cerebral infarction and the pathological changes of hippocampus in brain tissue were detected after 72 hours of modeling. Results Compared with the sham operation group

neurological deficit score

GRP78

PERK protein and mRNA expressions

as well as the expressions of e IF2α

chop and ATF4 at each time point in the model group increased. The volume of cerebral infarction increased（ P < 0. 01）. Compared with the model group

neurological deficit score

PERK protein and the mRNA expressions of PERK

e IF2α

chop and ATF4 decreased. GRP78 protein and the expression of mRNA increased. The volume of cerebral infarction decreased（ P < 0. 05 or P < 0. 01）.Conclusion Yangyin Tongnao Keli might inhibit endoplasmic reticulum stress by regulating the expressions of hippocampus endoplasmic reticulum related factors to decrease cerebral ischemia reperfusion injury.