Tianxiangdan Improves Coronary Microvascular Dysfunction in Rats by Inhibiting Microvascular Inflammation via Nrf2 Activation

Figure 5

TXD inhibited LPS-induced CMEC inflammation via activation of Nrf2. (a) Viability of CMECs after treatment with 50 μg/mL TXD and 10 μg/mL LPS, as well as pretreatment with 5 μM ML385 (Nrf2 inhibitor); (b and c) IL-1β and TNF-α expression in CMECs; (d) Immunofluorescence analysis of Nrf2 and NF-κB p65 expression in CMECs, scale bar = 20 μm; (e) Representative protein bands of Nrf2 and HO-1 and relative expression levels in CMECs; (f) Representative protein bands of IκBα, p-IκBα, NF-κB p65, and p-p65, and relative protein expression of p-IκBα and p-p65, in CMECs. or vs. control group; or vs. LPS group; or vs. LPS + TXD group. TXD, tianxiangdan granules; CMECs, cardiac microvascular endothelial cells; LPS, lipopolysaccharide.

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