| References: |
Leonurine can obviously attenuate the spontaneous excitatory postsynaptic current amplitude and frequency on pyramidal neurons[1]. Leonurine can dose-dependently suppress PI glycation. Leonurine may inhibit PI glycation through trapping MGO and keeping it from reacting with PI[2]. Leonurine can dose-dependently suppress PI glycation[3].Leonurine (60 mg/kg/day)+2-VO significantly decreases levels of glutamate and hydrogen peroxide, improves both the cognitive flexibility and the spatial learning and memory abilities. Moreover, leonurine obviously enhances long-term depression, elevates the ratio of N-methyl-D-aspartate receptor 2A/2B, and decreases the expression of postsynaptic density protein-95. Interestingly, the ratio of LC3II/LC3I and beclin-1 expression are markedly down-regulated by leonurine[1]. Leonurine significantly alleviates LPS-induced histopathological changes, downregulates the levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), upregulates the level of anti-inflammatory cytokine interleukin-10 (IL-10), and inhibits the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in mouse mastitis model. Leonurine inhibits the expression of Toll-like receptor 4 (TLR4) and the activation of nuclear factor-kappaB (NF-κB) and the phosphorylation of p38, extracellular signal-regulated kinase (ERK), and Jun N-terminal kinase (JNK)[4]. |
