The surface morphology of Platycodon grandiflorus polysaccharide and its anti-apoptotic effect by targeting autophagy
- Phytomedicine. 2022 Aug:103:154212. doi: 10.1016/j.phymed.2022.154212.
- 1. College of Veterinary Medicine, Shandong Agricultural University, Tai`an, Shandong 271018, China.
- 2. Ninth People's Hospital of Zhengzhou, Zhengzhou 450053, PR China.
- 3. Research Center for Animal Disease Control Engineering, Shandong Agricultural University, Tai`an, Shandong 271018, China.
- 4. Research Center for Animal Disease Control Engineering, Shandong Agricultural University, Tai`an, Shandong 271018, China. Electronic address: [email protected].
- 5. College of Veterinary Medicine, Shandong Agricultural University, Tai`an, Shandong 271018, China. Electronic address: [email protected].
Background: Fumonisin B1 is categorised as possible carcinogenic to humans which commonly contaminate maize and maize-based products worldwide, FB1, like Other environmental pollutants, may activate Apoptosis, Autophagy, the inflammatory response and oxidative stress. Platycodon grandiflorus polysaccharide (PGPSt) is prepared from a traditional herbal medicine in Asia with tremendous pharmacological activities. However, whether PGPSt could relieve FB1-induced Apoptosis has not been elucidated. The study aimed to evaluate the surface morphology of PGPSt and its protective effect on fumonisin B1-induced Apoptosis.
Methods: The surface morphology of PGPSt was evaluated by SEM and AFM. Expressions of proteins involved in Autophagy and Apoptosis were detected by western blot analysis. Western blot, transient transfection, JC-1 and Annexin V-FITC/PI staining, CCK8, Live-cell imaging and Autophagy inhibitor were used to observe the effect and explore the mechanism of PGPSt on FB1-induced Apoptosis of 3D4/21 cells.
Results: PGPSt had triple helix conformation, and had the characteristics of compact, polyporous and agglomerated morphology. PGPSt promoted the expression of LC3-II and Beclin1, reduced the expression of p62, and significantly activated Autophagy. PGPSt inhibited the Akt/mTOR signaling pathway at 24 h. Besides, PGPSt increased the expression of Bcl-2 and decreased the expression of Cleaved Caspase-3. PGPSt-mediated Autophagy was inhibited by 3-MA, accompanied by the upregulation of Caspase-3 and Cleaved Caspase-3, suggesting that enhanced Autophagy inhibited Apoptosis.
Conclusion: PGPSt can activate Autophagy, which in turn protects FB1-induced Apoptosis. Targeting Autophagy may provide a new way to improve the health of humans or Animals in FB1 contaminated areas.
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Research Areas: Cancer
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