In summary, our results indicated that Rh2 was able to ameliorate AD symptoms by inhibiting the production of TSLP in keratinocytes via inhibition of the NF-κB signaling pathway as well as by modulating Th2 cell differentiation and their effector function, possibly through the regulation of the expression of GATA3. Taken together, our results implied that Rh2 could potentially be applied as an effective therapeutic agent in the clinical management of AD. Here, NFKB1 is linked to Alzheimer disease.