Objective To explore the potential mechanism of Jili [Tribulus terrestris L. 蒺藜]in the treatment of hypertension. Methods The hypertension cell model was induced by angiotensin Ⅱ（ Ang Ⅱ） in the primary cultured hypothalamic neurons from neonatal Wistar rats. During the pharmacodynamics observation

the cells were divided into 5 groups: model group（ 2 × 10-6mol / L AngⅡ）

low dose Jili group（ preincubated with 3 μg / ml Jili for2 hours

then 2 × 10-6mol / L AngⅡ was added）

high dose Jili group（ preincubated with 30 μg / ml Jili for 2 hours

then 2 × 10-6mol / L AngⅡ was added）

Valsartan group（ preincubated with 10-5mol / L Valsartan for 2 hours

then2 × 10-6mol / L Ang Ⅱ was added） and control group（ with no intervention）. Then the cell number

the axonal length

the soma area

the survival rate and the apoptosis rate in each group were detected at the 24 th

48th and 72 nd hour after AngⅡ intervention. Also

the mRNA expression level of some cytokines

such as IκBα

IKK-α

IKK-β

NF-κB p65

JAK2

STAT3

AT1

GnRH

PKC and PI3 K

were detected at the 72 nd hour. During the pharmacological observation

the cells were divided into 6 groups: model group（ 2 × 10-6mol / L AngⅡ）

Jili group（ preincubated with 30 μg / ml Jili for 2 hours

then 2 × 10-6mol / L AngⅡwas added）

Valsartan group（ preincubated with 10-5mol / L Valsartan for 2 hours

then 2 × 10-6mol / L Ang Ⅱ was added）

antagonist group（ preincubated with 20 μmol / L TPCAK-1 for 2 hours

then 2 × 10-6mol / L AngⅡ was added）

Jili plus antagonist group（ preincubated with 30 μg /ml Jili and 20 μmol / L TPCA-1 for 2 hours

then 2 × 10-6mol / L AngⅡ was added） and control group（ with no intervention）. Then based on the results of pharmacodynamics observation

the action time of AngⅡ and the related cytokines were determined. Also

the expression level of mRNA and protein of related cytokines of each group were detected.Results Compared with those in the control group

the cell number

the soma area

the survival rate and the apoptosis rate in the model group increased significantly

while the axonal length deceased significantly at each time point after 24 hours after AngⅡ intervention; compared with those in the model group

the cell numbers

the soma areas

the survival rates and the apoptosis rates in the high dose Jili group and Valsartan group decreased significantly

while the axonal lengths increased significantly（ P < 0. 05）. Compared with those in the control group

the expression levels of IKK-β

NF-κB p65

JAK2

STAT3

AT1

GnRH

PKC and PI3 K increased significantly

while the levels of IKK-αand IκBα decreased significantly in the model group（ P < 0. 05）. Compared with those in the model group

the expression levels of IKK-β

NF-κB p65

JAK2

AT1

GnRH and PKC decreased

and the levels of IKK-α and IκBαincreased in the high does Jili group; the expression levels of IKK-β

NF-κB p65

AT1 and PKC decreased

and the levels of IKK-α and IκBα increased in the low does Jili group; the expression levels of IKK-β

NF-κB p65

AT1

GnRH and PKC decreased

and the levels of IKK-α and IκBα increased in Valsartan group（ P < 0. 05）. Based on the results above

the intervention time of AngⅡ was determined as 24 h

and the related cytokines were determined as IκBα

IKK-β

NF-κB p65 and NF-κB p50. Compared with those in the control group

the expression levels of the mRNA and the protein of IKK-β

NF-κB p50 and NF-κB p65 increased

while those of IκBα decreased in the model group; compared with those in the model group

the expressions of IKK-β

NF-κB p50 and NF-κB p65 decreased

while the expression of IκBα increased in Valsartan group and Jili group; compared with those in Valsartan group

the expressions of NF-κB p65 and IKK-β decreased

while the expression of IκBα increased in Jili group（ P < 0. 05）.Conclusion Jili could maintain the function of the blood pressure regulation center

and its potential mechanism of anti-hypertension might be related to regulating the IKK-β / NF-κB signaling pathway in hypothalamic neurons.