Adipose tissue- derived mesenchymal stem cells versus puerarin for ameliorating nicotine- induced pancreatic fibrosis in rats.

Chronic pancreatitis is a critical health problem that is usually complicated by pancreatic fibrosis and diabetes mellitus. Nicotine is a considerable etiological risk factor for this condition. Our research was constructed to explore and compare between the possible therapeutic roles of adipose tissue- derived mesenchymal stem cells (AT- MSCs) and puerarin (Pue) in improving nicotine-induced pancreatic fibrosis. Rats were randomly distributed into: group I; control rats and group II; nicotine- treated rats. Group II was further divided into; model, AT-MSCs- treated, Pue-treated and withdrawal groups. Weight gain study and intraperitoneal glucose tolerance tests were assessed. Pancreatic tissue was processed for measurement of amylase, lipase, interleukin- 6, malondialdehyde and superoxide dismutase. Furthermore, quantitative RT-PCR of caspase-3, transforming growth factor-beta1 (TGF- β1), alpha-smooth muscle actin (α-SMA) and collagen I, was performed. Histopathological, immunohistochemical and ultra-structural examinations were conducted as well. We found that administration of AT- MSCs and Pue helped to increase insulin secretion and suppress inflammatory oxidative stress parameters. In addition, apoptosis and fibrosis were receded through declining of caspase-3 and elements of TGF-β1/α-SMA/collagen I fibrotic pathway. The pancreatic architecture was restored to a great extent. However, AT-MSCs caused a marked pancreatic improvement and regeneration when compared to Pue which resulted in only a moderate amelioration. Insignificant and difficultly detectable spontaneous recovery was noticed in the withdrawal group. Both AT-MSCs and Pue have a promising effectiveness as targeted therapeutic agents against nicotine- induced pancreatic fibrosis, with a higher efficiency of AT- MSCs.