ArticleMolecular and cellular biochemistry2026
Octreotide attenuates pancreatic fibrosis through modulation of the HMGB1-Wnt/β-catenin axis in experimental chronic pancreatitis.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chronic pancreatitis is a progressive fibroinflammatory disease in which activated pancreatic stellate cells and extracellular matrix deposition drive irreversible tissue remodeling. Octreotide has anti-secretory and anti-inflammatory properties, but its anti-fibrotic mechanism remains unclear. To determine whether octreotide attenuates DBTC-induced pancreatic fibrosis through suppression of high-mobility group box 1 (HMGB1) and downstream Wnt/β-catenin signaling. Male Sprague-Dawley rats received dibutyltin dichloride (DBTC, 7 mg/kg) to induce chronic pancreatitis and were assigned to seven groups (n = 10/group) comprising untreated controls, DBTC model rats, and DBTC rats treated with octreotide alone or in combination with HMGB1 overexpression, HMGB1 knockdown, a vector control, or pharmacological Wnt/β-catenin activation. Octreotide was administered at 10 µg/kg/day for 21 days. Pancreatic injury, collagen deposition, stellate cell activation, HMGB1 inflammatory signaling, and Wnt/β-catenin activity were assessed by biochemical assays, histology, hydroxyproline measurement, immunofluorescence, Western blotting, qPCR, and ELISA. DBTC caused weight loss, pancreatic atrophy, elevated amylase/lipase, severe collagen accumulation, and marked increases in collagen I, α-smooth muscle actin (α-SMA), HMGB1, TLR4/RAGE, phospho-NF-κB p65, inflammatory cytokines, active/nuclear β-catenin, Wnt1, phospho-GSK3β, Axin2, c-Myc, and Cyclin D1 (all p < 0.0001 vs. Control). Octreotide substantially reversed these changes, halving fibrosis and hydroxyproline content and suppressing HMGB1 translocation/release (all p < 0.0001 vs. Model). HMGB1 overexpression weakened, whereas HMGB1 knockdown mimicked, octreotide-mediated protection. Wnt activation restored β-catenin activity and fibrosis without significantly changing HMGB1 or TLR4/RAGE/NF-κB signaling (all p > 0.15), a pattern consistent with HMGB1 acting upstream of Wnt/β-catenin. Octreotide limits experimental pancreatic fibrosis by suppressing HMGB1-driven inflammation and downstream Wnt/β-catenin activation, identifying the HMGB1-Wnt/β-catenin axis as a promising anti-fibrotic target.
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