This neuroprotective potential might be ascribed to the ability of BBN to regulate miR-181c-5p/HMGB1 axis or to inhibit the HMGB1/TLR4/NF-κB pathway to alleviate inflammation (Cao et al. 2020), and to promote the transformation of activated microglia from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype post-stroke (Zhu et al. 2018; 2019). This evidence concerns the gene TLR4 and stroke disorder.