Similar to the results in the T1DM mice model, oral administration of BefA reduced pancreatic inflammation by downregulating the expressions of TLR-4, p-NFκB/NFκB, IL-1β, and TNF-α, as well as promote the proliferation of islet β cells by lowering cell apoptosis (Bax/Bcl-2) and increasing the expression of PDX-1 (Figures 4 and 5). Here, BAX is linked to inflammatory response.