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It was shown recently that treatment of erythrocytes with bacterial neuraminidase leads to desialylation of the glycocalyx and provokes cell surface PS exposure [216]

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Treatment with TQ treatment (2.5, 5, and 10 mM) has been shown to suppress the NF-B-dependent neuroinflammation in the BV2 microglial cells, which is done by reducing the protein expression of iNOS, as well as inhibiting phosphorylation of IB, and preventing NF-B from binding to DNA