Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway

Yue Chen; Lu Lei; Kai Wang; Ruimin Liang; Yi Qiao; Zhijun Feng; Juanli Zhang; Min Bai; Haixia Chen; Jiaxin Zhao; Xingzhao Xiong; Jinyi Cao; Xia Shen; Zhifu Yang

doi:10.1155/2022/9496926

Huangqi-Honghua Combination Prevents Cerebral Infarction with Qi Deficiency and Blood Stasis Syndrome in Rats by the Autophagy Pathway

Evid Based Complement Alternat Med. 2022 Jan 24:2022:9496926. doi: 10.1155/2022/9496926. eCollection 2022.

Authors

Yue Chen^{1

2}, Lu Lei³, Kai Wang⁴, Ruimin Liang^{1

2}, Yi Qiao⁴, Zhijun Feng⁴, Juanli Zhang⁴, Min Bai^{1

2}, Haixia Chen^{1

2}, Jiaxin Zhao^{1

2}, Xingzhao Xiong⁵, Jinyi Cao², Xia Shen¹, Zhifu Yang²

Affiliations

¹ College of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
² Department of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
³ Department of Pharmacy, Xi'an Central Hospital, Xi'an 710003, China.
⁴ Department of Pharmacy, Xi'an Daxing Hospital, Xi'an 710016, China.
⁵ Department of Chemistry and Biochemistry, University of Delaware, Newark, DE 19716, USA.

Abstract

Background: Cerebral ischemia/reperfusion injury (CI/RI) contributes to the process of autophagy. Huangqi-Honghua combination (HQ-HH) is a traditional Chinese medicine (TCM) combination that has been widely used in the treatment of cerebrovascular diseases in China. The role of autophagy in HQ-HH-mediated treatment of CI/RI is unclear.

Methods: Sprague-Dawley (SD) rats were used to establish the middle cerebral artery occlusion (MCAO) with QDBS syndrome model and evaluate the function of HQ-HH in protecting against CI/RI.

Results: HQ-HH significantly improved the neuronal pathology and reduced infarct volume, neurological deficits, and whole blood viscosity in rats with CI/RI. Western blot results showed that the expression of autophagy marker proteins LC3II/LC3I and Beclin1 in the HQ-HH group was significantly lower than that in the model group, while the expression of p62 was significantly higher in the HQ-HH group as compared with the model group. There were no significant differences in PI3K, Akt, and mTOR levels between the HQ-HH group and the model group; however, p-PI3K, p-Akt, and p-mTOR were significantly upregulated. In addition, HQ-HH also changed the composition and function of intestinal flora in MCAO + QDBS model rats.

Conclusion: HQ-HH protects from CI/RI, and its underlying mechanism may involve the activation of the PI3K-Akt-mTOR signaling pathway, relating to the changes in the composition of intestinal flora.