Therefore, based on our findings, the potential mechanism of the Hsp-Cu(II) complex attenuated hyperuricemia and renal inflammation may related to inhibiting XO and ADA activities to reduce uric acid synthesis, regulating renal urate transport-related protein expression to promote uric acid excretion, reducing oxidative stress, and inhibiting the activation of NLRP3 inflammasome (Figure 9). Here, ADA is linked to hyperuricemia.