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已发表论文
芍药苷通过自噬减轻咪喹莫特诱导的系统性红斑狼疮小鼠的认知功能障碍和神经炎症
Authors Ma T, Wang Q, Zhang L, Chen X, Fan Z, Wang Y, Zhang X, Huang Y, Lu X, Song P, Xie C, Xi J, Li B, Wang Y
Received 28 March 2025
Accepted for publication 26 September 2025
Published 7 October 2025 Volume 2025:18 Pages 13945—13964
DOI https://doi.org/10.2147/JIR.S524710
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Ning Quan
Tianzhen Ma,1,2 Qian Wang,3 Liping Zhang,4 Xuan Chen,5 Zhiheng Fan,5 Yanxin Wang,3 Xiaonan Zhang,6 Yinjiu Huang,7 Xinghao Lu,8 Peipei Song,9 Changhao Xie,3 Jin Xi,2,10 Baiqing Li,11 Yuanyuan Wang1,2
1Department of Histology and Embryology, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 2Anhui Key Laboratory of Tissue Transplantation, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 3Department of Rheumatology and Immunology, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, 233004, People’s Republic of China; 4School of Public Health, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 5School of Clinical Medicine, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 6Department of Pathophysiology, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 7School of Life Science, Bengbu Medical University, Bengbu, 233000, People’s Republic of China; 8Department of Human Anatomy, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 9School of Mental Health, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 10Bengbu Medical University Research Center, Bengbu, Anhui, 233030, People’s Republic of China; 11Anhui Province Key Laboratory of Immunology in Chronic Diseases, Bengbu, Anhui, 233030, People’s Republic of China
Correspondence: Baiqing Li, Email baiqingli@bbmu.edu.cn Yuanyuan Wang, Email wangyuanyuantcm@bbmu.edu.cn
Purpose: This research was designed to systematically assess the neuroprotective efficacy of paeoniflorin and clarify the molecular mechanisms using two complementary models: a TLR-7 agonist imiquimod-induced murine lupus model and lipopolysaccharide-injured HT22 hippocampal neuronal cells.
Methods: A lupus-like phenotype was induced in C57BL/6J mice through topical administration of 1.25 mg 5% (w/w) imiquimod cream to the posterior auricular region three times a week for eight consecutive weeks, paeoniflorin by gavage for 7 days, and dexamethasone by intraperitoneal injection for 7 days. Animal behavioral experiments were performed at the end of the modeling. Subsequent execution of animals for biochemical analysis and histopathological examinations to evaluate the effects of paeoniflorin.
Results: Paeoniflorin ameliorated cognitive deficits, reduced autoantibody generation production, and hippocampal neuronal were observed in the SLE induced by the TLR-7 agonist imiquimod, accompanied by amelioration of blood-brain barrier damage. Subsequently, paeoniflorin activated autophagy and upregulated autophagy flux-related protein levels in mice with SLE induced by the TLR-7 agonist imiquimod. Interestingly, LPS-induced autophagy levels in HT22 cells were downregulated, but paeoniflorin pretreatment restored its autophagy inhibitory effect and attenuated the secretion of pro-inflammatory cytokines. Paeoniflorin activated the PI3K/AKT/mTOR pathway to restore autophagy, and using 3-methyladenine further confirmed the mechanism of paeoniflorin’s role in regulating autophagy.
Conclusion: Paeoniflorin plays a critical neuroprotective role as demonstrated in the TLR-7 agonist imiquimod-induced murine lupus model, mediated through activation of autophagic flux via modulation of the PI3K/AKT/mTOR signaling axis.
Keywords: cognitive, autophagy, neuroinflammation, paeoniflorin, NPSLE
1Department of Histology and Embryology, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 2Anhui Key Laboratory of Tissue Transplantation, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 3Department of Rheumatology and Immunology, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, 233004, People’s Republic of China; 4School of Public Health, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 5School of Clinical Medicine, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 6Department of Pathophysiology, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 7School of Life Science, Bengbu Medical University, Bengbu, 233000, People’s Republic of China; 8Department of Human Anatomy, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 9School of Mental Health, Bengbu Medical University, Bengbu, Anhui, 233030, People’s Republic of China; 10Bengbu Medical University Research Center, Bengbu, Anhui, 233030, People’s Republic of China; 11Anhui Province Key Laboratory of Immunology in Chronic Diseases, Bengbu, Anhui, 233030, People’s Republic of China
Correspondence: Baiqing Li, Email baiqingli@bbmu.edu.cn Yuanyuan Wang, Email wangyuanyuantcm@bbmu.edu.cn
Purpose: This research was designed to systematically assess the neuroprotective efficacy of paeoniflorin and clarify the molecular mechanisms using two complementary models: a TLR-7 agonist imiquimod-induced murine lupus model and lipopolysaccharide-injured HT22 hippocampal neuronal cells.
Methods: A lupus-like phenotype was induced in C57BL/6J mice through topical administration of 1.25 mg 5% (w/w) imiquimod cream to the posterior auricular region three times a week for eight consecutive weeks, paeoniflorin by gavage for 7 days, and dexamethasone by intraperitoneal injection for 7 days. Animal behavioral experiments were performed at the end of the modeling. Subsequent execution of animals for biochemical analysis and histopathological examinations to evaluate the effects of paeoniflorin.
Results: Paeoniflorin ameliorated cognitive deficits, reduced autoantibody generation production, and hippocampal neuronal were observed in the SLE induced by the TLR-7 agonist imiquimod, accompanied by amelioration of blood-brain barrier damage. Subsequently, paeoniflorin activated autophagy and upregulated autophagy flux-related protein levels in mice with SLE induced by the TLR-7 agonist imiquimod. Interestingly, LPS-induced autophagy levels in HT22 cells were downregulated, but paeoniflorin pretreatment restored its autophagy inhibitory effect and attenuated the secretion of pro-inflammatory cytokines. Paeoniflorin activated the PI3K/AKT/mTOR pathway to restore autophagy, and using 3-methyladenine further confirmed the mechanism of paeoniflorin’s role in regulating autophagy.
Conclusion: Paeoniflorin plays a critical neuroprotective role as demonstrated in the TLR-7 agonist imiquimod-induced murine lupus model, mediated through activation of autophagic flux via modulation of the PI3K/AKT/mTOR signaling axis.
Keywords: cognitive, autophagy, neuroinflammation, paeoniflorin, NPSLE