Mesenchymal stem cells (MSCs) have recently gained popularity as a treatment for a variety of diseases. In this work, bone marrow MSCs (BM-MSCs) and adipose MSCs (AD-MSCs) were compared to dexamethasone (Dex) in the management of colitis induced by acetic acid in rats. Rats were divided in a random way into five groups: (1) Control, (2) Acetic acid treated (2 ml of 3% of acetic acid solution, intra-rectally as a single dose), (3) BM-MSCs treated (single i.p. administration of 1×10 6 cells/rat, 24 hours after acetic acid exposure), (4) AD-MSCs treated (single i.p. administration of 1×10 6 cells/ rat, 24 hours after acetic acid exposure), and (5) Dex treated (0.5 mg/kg/, i.p., 1 hour after acetic acid exposure) for 7 days. Following that, after 15 days of colitis induction, all rats were decapitated. Acetic acid induced colitis was marked by elevation of edema marker, myeloperoxidase, malondialdehyde, interleukin-1β, tumor necrosis factoralpha,interleukin-6 apoptosis via caspase-3 expression, fibrosis using Masson's trichrome stain as well as infiltration of inflammatory cells by means of hematoxylin and eosin stain, It also lowered superoxide dismutase, total antioxidant, and interleukin-10 levels. After receiving either BM-MSCs or AD-MSCs, these adverse consequences were dramatically reduced. Finally, antioxidant, anti-inflammatory, antiapoptotic, and antifibrotic activities were detected in AD-MSCs, and BM-MSCs, indicating that they could be promising novel therapeutics for the treatment of colitis.

Background: Acute pancreatitis (AP) is a globally significant disease with increasing incidence and prevalence especially in the western world. It has severe complications such as pseudocyst, infection, renal failure, breathing problems, diabetes, malnutrition and chronic pancreatitis. Chronic pancreatitis can lead to pancreatic cancer which is one of the worst types of cancer. Up till now, there is no licensed specific treatment for AP. Objective: This study investigated the therapeutic effects of Mito-TEMPO in the treatment of L-Arginine induced acute pancreatitis in rats besides a possible involved mechanistic pathway. Materials and Methods: Rats randomly allocated into 3 groups: (1) control (received normal saline), (2) L-Arginine treated (300mg/100gm, i.p once) & (3) L-Arginine+Mito-TEMPO treated (0.7mg/kg/ day, i.p for 7 days). After 7 days from AP induction, serum amylase & lipase, pancreatic inflammatory mediators "toll-like receptor-4 (TLR-4), nuclear factor kappa-B (NF-кB), NLRP3 inflammasome, caspase-1, interleukin-1 beta (IL-1B)", oxidative parameters "malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO), reduced glutathione (GSH)", an apoptotic marker "caspase-3" & pancreatic histopathological changes were estimated for all rats.Results: L-Arginine induced AP was evidenced by elevation of serum amylase & lipase, pancreatic inflammatory mediators "TLR-4, NF-кB, NLRP3 inflammasome, caspase-1, IL-1B", oxidative parameters "MDA, MPO, NO", the apoptotic marker "caspase-3" and infiltration of inflammatory cells proved through hematoxylin & eosin stain alongside with the reduction of GSH content. All these harmful effects were improved significantly after the administration of Mito-TEMPO. Conclusion: Mito-TEMPO can be introduced as a new therapy for the treatment of acute pancreatitis due to its anti-inflammatory and antioxidant effects.

Objective: Acute pancreatitis (AP), a disorder of global importance, has a growing incidence and prevalence, particularly in the western world. Its complications include pseudo-cysts and chronic pancreatitis. Pramipexole (PMX), a D2/3 receptor selecting agonist used in Parkinsonism, has reported anti-inflammatory effects lately. Purpose: Exploring the potential curative role of PMX in an l-arginine-induced acute pancreatitis rat model besides a possible mechanistic pathway. Methods: Rats were divided randomly into three groups: control, l-arginine, and “l-arginine + PMX”. 7 days after AP induction, rats decapitated and estimated for serum amylase, lipase, glucose, pancreatic inflammatory mediators “toll-like receptor-4, nuclear factor- kappa B p65 ,serum tumor necrosis factor-α, NLRP3 inflammasome, caspase-1, interleukin-1 beta, oxidative biomarkers “malondialdehyde, myeloperoxidase, nitrite/nitrate, reduced glutathione, and the apoptotic marker “caspase-3”, with pancreatic histopathological changes. Results: L-arginine mediated AP proved by elevated serum lipase and amylase, pancreatic inflammatory, oxidative and apoptotic markers with infiltration of inflammatory cells using hematoxylin and eosin stain. PMX improved all these adverse signs of AP greatly. Conclusion: PMX might be considered as an innovative therapy for AP due to its remarkable antioxidant, anti-apoptotic, and anti-inflammatory effects, which are attributed to the suppression of the NLRP3 inflammasome and its downstream inflammatory cytokines.