Figure 8.

Pancreatic and systemic administration of miR-26a mimic ameliorates AP

(A) Schematic showing pancreatic ductal TLCS and miR-26a mimic administration regimens. (B) Levels of miR-26a in the pancreata with or without TLCS-AP. (C–E) Representative images (H&E; scale bar, 50 μm; magnification ×200) of pancreatic histopathology (C) and corresponding scores for edema, inflammatory cell infiltration, cell necrosis, and their sum value (D), serum amylase, lipase, and IL-6 levels (E) in TLCS-AP with or without miR-26a mimic. (F) Schematic showing intraperitoneal cerulein and miR-26a mimic administration regimens. (G) Levels of miR-26a in the pancreata with or without CER-AP. (H–J) Representative images (H&E; scale bar, 50 μm; magnification ×200) of pancreatic histopathology (H) and corresponding scores for edema, inflammatory cell infiltration, cell necrosis, and their sum value (I) as well as serum amylase and lipase levels (J). (K) Levels of Trpc3, Trpc6, autophagy (P62 and LC3), and inflammasome activation (Pro Casp-1 and Casp-1 p10) proteins in CER-AP pancreata with or without miR-26a mimic. (L) Summary diagram of the critical role of miR-26a in PAC [Ca²⁺]_i overload and its downstream pathological pathways, highlighting the therapeutic potential of miR-26a in AP. Data are from seven to nine mice per group, shown as mean ± SEM.