Patrinoside and Patrinoside A from Patrinia scabiosaefoli a Improve Insulin Resistance by Inhibiting NF- κ B, MAPK Pathways and Oxidative Stress in RAW264.7 and 3 T3-L1 Cells.
Zhenhua LiuMengke WangYuhang LiuMengjie RenXuefeng XiShiming LiWen-Yi KangPublished in: Oxidative medicine and cellular longevity (2023)
Patrinia scabiosaefolia , as traditional food and medicine plant, was used to treat appendicitis, enteritis, and hepatitis for thousand years in China. Patrinoside and patrinoside A isolated from P. scabiosaefolia could significantly improve insulin resistance (IR) by activating PI-3 K/AKT signaling pathway in our previous study. Since IR is closely related to inflammation, their anti-inflammatory activities in RAW264.7 inflammatory model induced by LPS and in 3 T3-L1 IR inflammatory model induced by TNF- α were evaluated to identify whether the effects on improving IR related to anti-inflammatory activity. In RAW264.7 cells, patrinoside and patrinoside A significantly inhibited the transcription and secretion of inflammatory mediators NO, TNF- α , and IL-6. Western blot analysis showed that the significant inhibition of phosphorylation of I κ B and P65 and P38, ERK and JNK suggested that the effects were exerted through NF- κ B pathway and MAPK pathway. In 3 T3-L1 cells, patrinoside and patrinoside A also inhibited the activation of NF- κ B and MAPK pathways through inhibiting the transcriptions of inflammatory cytokines IL-6 and chemokines MCP-1 and MIP-1 α . These events resulted in the inhibition of macrophages migration to adipocytes. In addition, patrinoside and patrinoside A ameliorated oxidative stress by inhibiting ROS release in LPS-stimulated RAW264.7 cells. In conclusion, patrinoside and patrinoside A could active PI-3 K/AKT pathway, inhibit NF- κ B pathway, MAPK pathway, and improve oxidative stress, which showed multipathways on improving IR. These results provided the scientific basis for material basis and mechanism on improving IR of P. scabiosaefolia .
Keyphrases
- signaling pathway
- induced apoptosis
- pi k akt
- cell cycle arrest
- oxidative stress
- epithelial mesenchymal transition
- insulin resistance
- anti inflammatory
- adipose tissue
- dna damage
- type diabetes
- endoplasmic reticulum stress
- rheumatoid arthritis
- metabolic syndrome
- cell proliferation
- diabetic rats
- inflammatory response
- immune response
- high fat diet
- human health
- high fat diet induced
- nuclear factor
- heat stress