TH and metabolic disease: Results suggested that the potential mechanisms of XBXD against CINV may in large part be due to the regulation of 5-HT synthesis and metabolism disorders and the blockade of 5-HT3R. Besides, XBXD significantly inhibited tyrosine hydroxylase (TH), a synthetic rate-limiting enzyme of DA (Daubner et al., 2011), to reduce the overexpression of DA and block the peripheral D2R, which may be another antiemetic mechanism of XBXD (Yu et al., 2015b; Yu, 2015).