In summary, this study revealed that ACT can effectively inhibit Müller cell reactive proliferation and alleviate retinal dysfunction in DR rats and that the specific therapeutic molecular mechanism involves ACT inhibiting Müller cell reactive hyperplasia by regulating TXNIP and mediating the expression of the Kir4.1 channel in a PI3K/Akt-dependent manner to alleviate diabetic retinopathy. Here, TXNIP is linked to diabetic retinopathy.