Objective: To explore the therapeutic effect of TanIIA on PAH and its possible mechanism through hypoxic-induced PAH mice and cell models. Methods: C57BL6 male mice were randomly divided into the normal oxygen group (5 mice)

the hypoxia group (5 mice)

and the hypoxia + TanIIA group (5 mice). After 4 weeks

right ventricular pressure was detected by right heart catheter. HE staining of lung tissue was performed. MDA and SOD in lung tissues were detected by TBA and WST-8 methods. hPASMCs cells were randomly divided into the normal oxygen group

hypoxic group and hypoxic +TanIIA group. 24 hours later

the protein expression levels of Bax

P62

Akt and P-Akt were detected by WB experiment. Results: The right ventricular systolic pressure was increased in the hypoxic group compared with the normal oxygen group (P<0.05)

and decreased in the hypoxic +TanIIA group compared with the hypoxic group (P<0.05).Compared with the normal oxygen group

the pulmonary vascular remodeling degree of the hypoxia +TanIIA group was significantly reduced compared with the hypoxia group. SOD and MDA in lung tissues of the hypoxic group and the hypoxic +TanIIA group increased and MDA decreased compared to the normal oxygen group (P<0.05). Compared with normal oxygen group

Bax protein expression in PASMCs decreased and P62 protein expression increased in hypoxia group (P<0.05).Compared with the hypoxia group

Bax protein expression in PASMCs increased and P62 protein expression decreased in the hypoxia +TanIIA group (P<0.05).The p-Akt/Akt ratio in PASMCs was increased in the hypoxic group compared with the normal oxygen group (P<0.05)

and the P-Akt/Akt ratio was decreased in the hypoxic + TanIIA group compared with the PASMCs in the hypoxic +TanIIA group (P<0.05). Conclusion: TanIIA can protect hypoxic PAH

which may be related to reducing the oxidative stress level in hypoxic PAH

inhibiting the activation of PI3K/Akt signaling pathway in hypoxic PASMCs

and improving pulmonary vascular remodeling in PAH.