C-Phycocyanin and Lycium barbarum Polysaccharides Protect against Aspirin-Induced Inflammation and Apoptosis in Gastric RGM-1 Cells.
Yu-Chen LiuChun-Chao ChangHirofumi MatsuiJane C-J ChaoPublished in: Nutrients (2022)
Aspirin causes gastrotoxicity and damaged epithelial defense via cyclooxygenase inhibition. C-phycocyanin (CPC) and Lycium barbarum polysaccharides (LBP), an active ingredient of Spirulina platensis and wolfberry, respectively, exerted antioxidation, anti-inflammation, and/or immunoregulation. The actions of CPC and/or LBP on gastric damage induced by aspirin were explored in rat gastric mucosal RGM-1 cells. Gastric injury was performed by 21 mM aspirin for 3 h after the pretreatment of CPC and/or LBP (100-500 μg/mL) for 24 h in RGM-1 cells. Proinflammatory, anti-inflammatory, and apoptotic markers were examined by ELISA or gel electrophoresis and Western blotting. Cell viability and interleukin 10 (IL-10) were reduced by aspirin. Increased proinflammatory markers, caspase 3 activity, and Bax protein were observed in RGM-1 cells with aspirin treatment. Aspirin elevated nuclear factor-κB (NF-κB), extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) activation, while CPC and/or LBP increased IL-10, and attenuated proinflammatory markers, Bax protein, NF-κB, and the activation of ERK and JNK. Therefore, CPC and/or LBP possess anti-inflammation by restraining the activation of the ERK signaling pathway, and LBP decreases apoptosis by suppressing the JNK signaling pathway activation in gastric RGM-1 cells with aspirin-induced epithelial damage.
Keyphrases
- induced apoptosis
- signaling pathway
- oxidative stress
- cell cycle arrest
- pi k akt
- endoplasmic reticulum stress
- low dose
- cell death
- diabetic rats
- cardiovascular events
- epithelial mesenchymal transition
- antiplatelet therapy
- nuclear factor
- immune response
- cardiovascular disease
- anti inflammatory
- percutaneous coronary intervention
- type diabetes
- south africa
- high glucose
- nitric oxide
- lps induced
- protein protein