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The peptide upregulates MMP-2 expression in dermal fibroblasts by 85%, facilitating breakdown of damaged collagen and enabling cellular migration through dense matrix environments, while simultaneously enhancing production of tissue inhibitors of metalloproteinases (TIMPs) to prevent excessive degradation

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Results We demonstrated that this peptide-liposome-small molecule machinery targets AML and consequently induces cell apoptosis both in vitro and in vivo through three disparate mechanisms: (I) Oridonin, as a Michael acceptor molecule, inhibits GSH function through covalent bonding, triggering an initial imbalance of oxidative stress