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It has been shown that HSYA was able to significantly protect the liver from oxidative stress by increasing the activities of antioxidant enzymes, upregulating the expression of PPAR- and MMP-2, and downregulating the expression of TGF-1 and tissue inhibitor of metalloproteinases-1 (TIMP-1), and reducing -SMA level, which indicating that PPAR-TGF-1 would be a signal pathways for HSYA to reduce liver fibrosis induced by oxidative stress (Wang et al., 2013)
BPC-157 has been investigated for its relationship to pro-inflammatory and anti-inflammatory signals in gut and tissue models
Intravascular hemolysis activates complement via cell-free heme and heme-loaded microvesicles
The GLP space is evolving beyond single-pathway thinking
T4 stage and preoperative anemia as prognostic factors for the patients with colon cancer treated with adjuvant FOLFOX chemotherapy
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