4.7 Article

Inhibitory regulation of purple sweet potato polysaccharide on the hepatotoxicity of tri-(2,3-dibromopropyl) isocyanate

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ELSEVIER
DOI: 10.1016/j.ijbiomac.2021.11.086

关键词

Purple sweet potato polysaccharide; Tris-(2,3-dibromopropyl) isocyanurate; Apoptosis; Mitochondrial pathway; Death receptor pathway

资金

  1. Heilongjiang Provincial Natural Science Foundation of China [LH2020H036]
  2. Outstanding Young Talents Project of the Central Government's Reform and Development Fund for Local Universities [2020YQ12]
  3. Heilongjiang Pro-vincial Scientific Research Project of Basic Scientific Research [2020CX09]
  4. Scientific Research Project of Heilongjiang Provincial Health Commission [2019-021]
  5. Scientific Innovation Fund of First Affiliated Hospital of Harbin Medical University [2020L04]

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This study demonstrated the protective effect of Purple Sweet Potato Polysaccharide (PSPP) on Tri-(2,3-dibromopropyl) isocyanate (TBC) induced liver injury, providing a scientific basis for further research on the hepatotoxic mechanism of TBC and the protective effect of PSPP.
Tri-(2,3-dibromopropyl) isocyanate (TBC), a new emerged persistent organic pollutant, is widely used in fields of flame retardant, textile, rubber and plastic with strong hepatotoxicity. Purple Sweet Potato Polysaccharide (PSPP) has antioxidant and hepatoprotective effects. This study aims to answer the scientific question whether PSPP has a protective effect on TBC induced liver injury. The effect of PSPP on the apoptosis of HepG2 cells was detected by MTT assay, the morphological changes were observed by morphological observation, and the apoptosis rate was determined by flow cytometry. The apoptotic genes were detected by qPCR assay, the relevant protein express was detected by western blot. The correlation between proteins and genes in the apoptosis pathway of HepG2 cells was calculated. To further reveal the apoptosis mechanism of TBC hepatotoxicity in vivo, 19 target genes and 14 apoptotic related proteins of inhibiting apoptosis via death receptor and mitochondria were discussed, all the above results proved that PSPP had protective effect on liver injury induced by TBC. This study not only provided a scientific basis for clarifying the mechanism of TBC hepatotoxicity and the protective effect of PSPP, but also generated the new point and method in terms of the prevention in advance and early intervention of diseases caused by environmental pollution.

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