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Results clearly showed that the tyrosine-nitration level was reduced in proportion to the molar ratios of GSSSG and LASSS relative to HGF, as revealed by the decrease in anti-nitroY mAb-positive HGF (60-kDa -chain and 90-kDa proform) normalized to total HGF -chain as a loading control, that was monitored by stripping with SDS-ME solution and re-probing the blot with anti-HGF -chain N-terminal domain mAb (Figure 1b,c, second and third rows)

In other words, in addition to inhibiting the expression of p-STAT3, GHK-Cu likely targets other pathways that inhibit the expression of inflammatory factors

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