Fig 2: Effects of sotagliflozin on cardiac inflammation in post-MI rats. (A) Representative images of heart tissue stained with Sirius red or CD68 fluorescent antibody (green) and DAPI (blue) from post-MI rats treated with sotagliflozin or saline. (B) Western blot analysis of the NLRP3 pathway markers (NLRP3, IL-18, and IL-1β) in the peri-infarction region of the heart. (C) Western blot analysis of NF-κB pathway markers (p-P65, TNF-α) in the peri-infarction region of the heart. Data are expressed as the mean ± SEM; n ≥ 3 in each group. *p < 0.5. Sota: sotagliflozin.

Fig 3: Inactivation of the PI3K‐AKT pathway abrogates the relieving impacts of BMSC‐Exos on DOX‐induced OS and pyroptosis in H9C2 cells. (A, B) DCFH‐DA staining to measure ROS levels in cells. (C, D) JC‐1 immunofluorescence to monitor the changes of potential difference of mitochondrial membrane in cells. (E, F) Western blot to test the expression of NLRP3, ASC, cleaved caspase‐1, NT‐GSDMD, cleaved IL‐1β, and cleaved IL‐18 in cells. (G, H) Western blot to measure the phosphorylation levels and total protein levels of Foxo1 in cell nucleus and cytoplasm; ***p < .001 versus the control group; ## p < .01; ### p < .001 versus the DOX group; & p < .05; && p < .01; &&& p < .001 versus the DOX + BMSC‐Exo group. One‐way analysis of variance was adopted to confirm p values, with Tukey's test for post hoc multiple comparisons. Each experiment was independently repeated thrice. AKT, protein kinase B; ASC, apoptosis‐associated speck‐like protein containing A CARD; BMSC, bone marrow stromal cells; DCFH‐DA, 20,70‐dichlorofluorescein diacetate; DOX, doxorubicin; Exo, exosome; Foxo1, forkhead box O1; GSDMD, gasdermin D; IL, interleukin; NLRP3, nucleotide‐binding oligomerization domain, leucine rich repeat and pyrin domain containing 3; OS, oxidative stress; PI3K, phosphatidylinositol 3‐kinase; ROS, reactive oxygen species.

Fig 4: Representative IHC staining images showing immunoreactivity A–D(A) Score 0, (B) score 1, (C) score 2, and (D) score 3 of TMPRSS2, IL18, and AhR in lung cancer tissue. Scale bars, 2.5 mm (low magnification) and 100 μm (high magnification). Source data are available online for this figure.

Fig 5: Expression levels of TMPRSS2 and nuclear AhR in normal and cancer lung tissues IHC staining of TMPRSS2, IL18, and nuclear AhR in a representative normal lung tissue section. Scale bars, 2.5 mm (low magnification) and 100 μm (high magnification).IHC staining of TMPRSS2, IL18, and nuclear AhR in lung cancer tissues that displayed high or low expression of TMPRSS2. Scale bars, 2.5 mm (low magnification) and 100 μm (high magnification).A schematic representation summarizing the mechanism by which particulate matter upregulates TMPRSS2 to promote lung cancer progression. Source data are available online for this figure.