Rat Pancreas Research Articles

Histological and biochemical effects of an ethanolic extract of Myrtus communis leaf on the pancreases of rats fed high fat diets

ABSTRACT We investigated the effects of an ethanolic extract of Myrtus communis subsp. communis (MC) leaves on the pancreases of rats fed with a high fat diet (HFD). Wistar albino rats were fed either with standard lab chow (Control group) or with a 45% fat diet (HFD and HFD+MC groups) for 4 months, with the MC extract (100 mg/kg) being administered by orogastric gavage to rats in the HFD+MC group during the last month. Blood and pancreas samples were collected from all experimental groups at the end of the study. Insulin and leptin levels, and the lipid profile, were analyzed in the blood serum. Pancreatic injury was assessed histologically. Insulin, nuclear factor kappa beta (NF-κB), and alpha-smooth muscle actin (α-SMA) were assessed using immunohistochemistry. Apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) immunohistochemistry. In addition, oxidant/antioxidant activity was analyzed by biochemical methods. Increased body weight, serum insulin and leptin levels, blood glucose level and pancreatic tissue malondialdehyde (MDA), 8-hydroxy-2’-deoxyguanosine (8-OHdG) levels, myeloperoxidase (MPO) activity and decreased tissue glutathione (GSH) level were observed in the HFD group compared to the Control group, in addition to dyslipidemia. An increased histopathological damage score, pancreatic islet area, insulin, TUNEL, NF-κB and α-SMA immunoreactivity were seen in animals from the HFD group compared to the Control group. However, such pathological changes were reduced in the HFD+MC group. Our data indicate further investigation of MC extract as a therapeutic adjuvant for HFD-induced pancreatic injury, acting via anti-inflammatory and antioxidant mechanisms, is worth carrying out.

Comparative Analysis of Epigallocatechin-3-Gallate and TNF-Alpha Inhibitors in Mitigating Cisplatin-Induced Pancreatic Damage Through Oxidative Stress and Apoptosis Pathways

Oxidative stress and inflammation caused by cisplatin, which is frequently used in the treatment of many cancers, damage healthy tissues as well as cancer cells. In this study, we aimed to investigate the effect of epigallocatechin-3-gallate (EGCG) and infliximab (INF) administration on pancreatic endocrine cells in rats treated with systemic cisplatin (CDDP). The rats were randomly divided into 6 groups: group 1 (control group), group 2 (EGCG group), group 3 (CDDP group), group 4 (EGCG + CDDP group), group 5 (CDDP + INF group), and group 6 (EGCG + CDDP + INF group). The study’s findings demonstrated that EGCG and INF effectively reduced the cellular damage induced by CDDP in histopathologic investigations of the pancreas. EGCG and INF, whether used individually or in combination, demonstrated a significant reduction in malondialdehyde (MDA) levels and an increase in glutathione (GSH) levels in the rat pancreas compared to the CDDP group. Immunohistochemically, the enhanced presence of insulin and glucagon positivity in the EGCG and INF groups, along with the absence of TUNEL immunopositivity, indicate that both treatments reduced CDDP-induced apoptosis. Furthermore, the observed lack of immunopositivity in TNF-α and 8-OHdG in the groups treated with EGCG and INF, compared to those treated with CDDP, indicates that these substances can inhibit inflammation. EGCG and INF, whether provided alone or together, can potentially reduce the damage caused to pancreatic islet cells by cisplatin. This effect is achieved through their anti-inflammatory and antioxidant properties during the early stages of the condition.

Among Other Tissues, Short-Term Garlic Oral Treatment Incrementally Improves Indicants of Only Pancreatic Islets of Langerhans Histology and Insulin mRNA Transcription and Synthesis in Diabetic Rats.

The source, mRNA transcription, and synthesis of insulin in the pancreas, in addition to the bile duct and liver, in streptozotocin (STZ)-induced diabetic rats (DR) in response to garlic oral treatment are not yet clear. This study investigated the accumulative effects of continued garlic oral treatment on changes in the pancreas, bile duct, and liver with regards to: 1-Insulin mRNA transcription, synthesis, and concentration in relation to changes in serum insulin (SI); 2-Insulinogenic cells insulin intensity and distribution, proliferation, and morphology. Fasting blood glucose (FBG) and insulin concentration in serum and pancreas (PI) and sources and mRNA transcription in the pancreas, bile duct, and liver in normal rats given normal saline (NR-NS) and DR given either NS (DR-NS) or garlic extract (DR-GE) before and after 1, 4, and 8 weeks of oral treatment were examined. Compared to NR-NS, DR-NS showed a significant increase in FBG and reductions in SI and PI and deterioration in islets histology, associated pancreatic insulin numerical intensities, and mRNA transcription. However, compared to DR-NS, the targeted biochemical, histological, and genetic variables of DR-GE were significantly and incrementally improved as garlic treatment continued. Insulin or its indicators were not detected either in the bile duct or the liver in DR-GE. 8 weeks of garlic oral treatment is enough to incrementally restore only pancreatic islets of Langerhans insulin intensity and insulinogenic cells proliferation, morphology, and distribution. These indices were associated with enhanced pancreatic insulin mRNA transcription and synthesis. Eight weeks of garlic treatment were not enough to stimulate insulinogenesis in either the bile duct or the liver.

Pancreatic and hepatic histopathology of high-fat diet fed streptozotocin-induced Wistar rat model of type 2 diabetes mellitus

In search of new fangled therapeutic agents against type 2 diabetes mellitus (T2DM), an appropriate preclinical disease model is important to ensure the success of subsequent clinical trials. There is an increasing trend in the use of high-fat diet (HFD) fed streptozotocin (STZ)-induced rodent models in investigating novel therapeutic agents against T2DM. Though several studies have been conducted on the development of the aforementioned model they were mainly focused on biochemical characteristics. Only limited studies have focused on histopathological changes which is the gold standard in investigating the treatment-related changes of novel therapeutic agents. Therefore, the present study aimed at assessing the histopathological changes of the pancreas and liver, the two main organs involved in glucose homeostasis, in a newly developed HFD-fed STZ-induced Wistar rat model. For this study, Wistar rats were induced with T2DM by intraperitoneal injection of STZ (30, 40, and 50 mg/kg) which was given after feeding the rats with an HFD consisting of 60% calories from fat for four weeks duration. Diabetic rats were sacrificed after maintaining for further four weeks. The liver and pancreas were excised and hematoxylin and eosin-stained sections were observed using a light microscope. The major histopathological changes in the pancreas of HFD-fed STZ-induced diabetic rats were loss of pancreatic islets, pancreatic islet hypertrophy, and mild fatty change in the exocrine pancreas. In contrast, the liver did not show any degree of fatty change, but the majority showed prominent hydropic degeneration in the hepatocytes. In conclusion, prominent alterations were well noted in the pancreatic and liver tissues of the Wistar rats fed with HFD, followed by STZ (50 mg/kg), and the established model could be useful in investigating and elucidating antidiabetic mechanisms of novel pharmaceutical agents.

Changes of RNA m6A/m5C Modification Regulatory Molecules in Ferroptosis of T2DM Rat Pancreas.

N6-methyladenine (m6A) and 5-methylcytosine (m5C) are two common forms of RNA methylation that play an important role in the epigenetics of type 2 diabetes mellitus (T2DM). One type of cell death, ferroptosis, has been implicated in islet β-cell damage in T2DM. Notably, RNA methylation, an upstream regulatory mechanism of mRNAs, can regulate the expression of ferroptosis signaling molecules, thereby affecting cell proliferation and death. Here, we found that the ferroptosis signaling pathway was activated in pancreas of T2DM rats, followed by significant changes in m6A/m5C modification regulatory molecules. These detection data together with the prediction results that m6A and m5C exist in the mRNAs of ferroptosis molecules, we speculate that m6A and m5C are probably involved in pancreatic cell damage by modifying of ferroptosis signaling molecules. In short, our findings provide a new research idea for future studies on the molecular mechanisms of pancreatic cell damage and point to a new direction for exploring the mechanisms of ferroptosis from the perspective of RNA methylation modification.

Effect of Aqueous Solanum macrocarpon Leaves Extract on Hyperglycemia, Liver Enzymes, and Liver and Pancreas Histology in Alloxan-Induced Diabetes

Solanum macrocarpon (SM) is frequently used for both medicinal and dietary purposes. It has been documented to have hypoglycemic properties in diabetes management. This research delved into the effect of aqueous Solanum macrocarpon leaves extract on blood glucose levels, liver enzymes, antioxidant enzymes, and histology of the liver and pancreas in alloxan-induced diabetic rats. A total of thirty male Wistar rats, with weights ranging from 150 to 200 g, were randomly divided into six groups, each containing five rats. The normal (A) and diabetic control (B) groups received distilled water. The diabetic treated groups (C, D, E, and F) were administered 5 mg of glibenclamide, 250 mg/kg, 500 mg/kg, and 750 mg/kg of Solanum macrocarpon extract orally for a period of 14 days. Significant reversal of the altered levels of liver enzymes was noted in the results. Positive alterations in blood glucose concentration and antioxidant enzyme activity were also observed. The histological examination showed damage to the hepatic and pancreatic cells of the diabetic untreated rat group, which was mitigated in diabetic rats treated with the aqueous extract. The findings indicate that the aqueous Solanum macrocarpon leaves extract serves as a valuable source of natural antioxidants, promoting both liver function and blood glucose regulation.

Material basis and molecular mechanisms of Chaihuang Qingyi Huoxue Granule in the treatment of acute pancreatitis based on network pharmacology and molecular docking-based strategy.

This study aimed to analyze active compounds and signaling pathways of CH applying network pharmacology methods, and to additionally verify the molecular mechanism of CH in treating AP. Network pharmacology and molecular docking were firstly used to identify the active components of CH and its potential targets in the treatment of AP. The pancreaticobiliary duct was retrogradely injected with sodium taurocholate (3.5%) to create an acute pancreatitis (AP) model in rats. Histological examination, enzyme-linked immunosorbent assay, Western blot and TUNEL staining were used to determine the pathway and mechanism of action of CH in AP. Network pharmacological analysis identified 168 active compounds and 276 target proteins. In addition, there were 2060 targets associated with AP, and CH had 177 targets in common with AP. These shared targets, including STAT3, IL6, MYC, CDKN1A, AKT1, MAPK1, MAPK3, MAPK14, HSP90AA1, HIF1A, ESR1, TP53, FOS, and RELA, were recognized as core targets. Furthermore, we filtered out 5252 entries from the Gene Ontology(GO) and 186 signaling pathways from the Kyoto Encyclopedia of Genes and Genomes(KEGG). Enrichment and network analyses of protein-protein interactions predicted that CH significantly affected the PI3K/AKT signaling pathway, which played a critical role in programmed cell death. The core components and key targets showed strong binding activity based on molecular docking results. Subsequently, experimental validation demonstrated that CH inhibited the phosphorylation of PI3K and AKT in pancreatic tissues, promoted the apoptosis of pancreatic acinar cells, and further alleviated inflammation and histopathological damage to the pancreas in AP rats. Apoptosis of pancreatic acinar cells can be enhanced and the inflammatory response can be reduced through the modulation of the PI3K/AKT signaling pathway, resulting in the amelioration of pancreatic disease.

Moringa oleifera gum effect on blood sugar levels and rat pancreas histology induced by Streptozotocin

Moringa gum is a product that people can use as an anti-hyperglycemic agent. This study aimed to determine the effectiveness of Moringa gum in reducing blood sugar levels and improving the histology structure of the rat pancreas induced by streptozotocin (STZ). This study used 21 male rats divided into 3 groups including control, diabetes (STZ), and diabetes (STZ + 3% Moringa gum). STZ treatment at a single dose (45 mg/kg BW) was given intraperitoneally, while Moringa gum was given through drinking water for 2 weeks. Blood sugar levels were measured on days 0, 7th, 14th, 21st, and 28th. The results showed that STZ administration induced diabetes in rats with blood sugar levels of 487 mg/dL on the 14th day. Moringa gum administration was able to reduce blood sugar levels on days 21st and 28th respectively to 306 and 234 mg/dl. The histology structure of the pancreas of rats treated with gum also showed improvement. This study concludes that Moringa gum is effective in lowering blood sugar levels in rats even though it still does not show normal blood sugar levels, and can repair STZ-induced damage to the histology structure of the rat pancreas.

Characteristic of a group of genes with low level of expression in the pancreas of rats under conditions of multi-day intermittent hypoxia influence

In modern medical science great attention is paid to the clarification of the molecular mechanisms, which are the basis of adaptation to environmental factors of unusual origin and/or extraordinary strength. The aim of the study is to determine the features of a group of genes with low expression level, associated with hypoxia in the pancreas of Wistar rats under conditions of intermittent hypoxia. Materials and methods. The study was conducted on 10 white, sexually mature Wistar rats, which were divided into 2 groups (5 animals in each). Animals of group 1 were part of the control (intact) group. The animals of the 2nd group were subjected to hypoxic training according to the following scheme: for 15 days, 6 hours daily, namely on days 1–5 they simulated an ascent to a height of one to five kilometers above sea level under the conditions of a barometer, and the last 10 days 6 km above the sea level. To analyze gene expression, we used the polymerase chain reaction method with real-time reverse transcription (PCR) CFX-96 Touch™ (Bio-Rad, USA) and the RT2 Profiler™ PCR Array Rat Hypoxia Signaling Pathway kit (QIAGEN, Germany), where 84 genes were the subject of research in experimental animals. Results. According to the results of the PCR study of genes in the pancreas samples of intact animals and animals exposed to hypoxic training, it was established that out of 84 genes associated with hypoxia, a group of 5 genes with a low expression level (∆∆Ct < 30) was found. This pattern includes Bhlhe40 genes, Ctsa, Hif1a, Lox, and Slc16a3, the expression of which is statistically reduced. Thus, compared to the level of their expression in intact animals, the expression of Bhlhe40 decreased by 2.59 times, Ctsa by 6.02 times, Hif1a by 3.85 times, Lox by 3.01 times, and Slc16a3 by 2.40 times. Conclusions. Intermittent hypoxia reduces the expression of the Bhlhe40 gene by 2.59 times, which can be considered as an element of adaptation of cells to a low level of oxygen and modulation of genetic programs. The decrease in Ctsa gene expression by 6.02, Hif1a by 3.85, and Lox by 3.01 times during intermittent hypoxia demonstrates, that these effects can be used as sanogenic factors in insulin resistance and type 2 diabetes. The 2.40-fold decreased expression level of Slc16a3 is probably an element of metabolic adaptation and adaptation of the metabolic pathway of cells to hypoxia conditions.

Da-Cheng-Qi decoction improves severe acute pancreatitis capillary leakage syndrome by regulating tight junction-associated proteins.

To investigate mechanisms underlying the effects of Da-Cheng-Qi decoction (DCQD) on severe acute pancreatitis (SAP) capillary leakage syndrome. In this study, a SAP rat model was established using retrograde perfusion of 5% sodium taurocholate into the biliopancreatic duct. The study included three randomized groups: control, SAP (modeling), and DCQD (via gavage at 2h pre-modeling and 2 and 4h post-modeling). HPLC was used to analyzed major components of DCQD. Pathological changes and capillary permeability in the rat pancreatic tissues were examined. mRNA levels of claudin 5, occludin, zonula occludin-1 (ZO-1), and junctional adhesion molecules (JAM-C) were assessed using qRT-PCR. Tight junction-associated protein expression was evaluated using immunofluorescence and Western blot analyses. Human umbilical vein endothelial cells (HUVECs) were used to investigate the mechanism m of DCQD. Serum levels of amylase, TNF-α, IL-1β, IL-2, and IL-6 were higher in the SAP group compared to the DCQD group (p < 0.05). DCQD treatment significantly attenuated rat pancreas damage (p < 0.05) and reduced tissue capillary permeability compared to the SAP group (p < 0.05). Claudin 5, occludin, and ZO-1 expression in the rat tissues was upregulated, but JAM-C was downregulated by DCQD treatment (p < 0.05). HUVEC permeability was improved by DCQD in a dose-time-dependent manner compared to the SAP group (p < 0.05). DCQD also upregulated claudin 5, occludin, and ZO-1 expression in vitro (p < 0.05). DCQD can improve capillary permeability in both in vivo and in vitro models of SAP by upregulating expression of claudin 5, occludin, and ZO-1, but not JAM-C.

Kigelia africana (Lam.) Benth. fruit inhibits iron-induced lipid peroxidation and ?-amylase enzyme activity

Insufficiencies in insulin secretion and/or action cause diabetes mellitus (DM), a complex condition characterized by abnormal blood glucose levels. Diabetes is often treated by modifying either glucose metabolism, lipids metabolism, or both. A direct correlation has been found between high levels of lipid peroxide in individuals with diabetes and lower intracellular antioxidant activity. Therefore, this study was designed to investigate the effect of the aqueous extract of Kigelia africana fruit on the carbohydrate hydrolyzing enzyme, ?-amylase, and FeSO4-induced lipid peroxidation in the rat pancreas. The in vitro antioxidant potential, including assays for (1,1 diphenyl-2-picryl hydrazyl (DPPH), ferric reducing antioxidant property (FRAP), nitric oxide (NO), hydroxyl (OH) scavenging, and Fe2+ chelating abilities, of the fruit extract was also evaluated. The effect of the fruit extract on the ?-amylase enzyme, and FeSO4-induced lipid peroxidation in the rat pancreas was also evaluated. K. africana at a concentration of 0.5 mg/mL and 1 mg/mL scavenged DPPH radicals, with the lower concentration showing significant differences compared to the control. The K. africana fruit extract reduced ferric compounds significantly compared to the standard. The OH* radical scavenging results revealed that all concentrations of K. africana fruit scavenged OH* radicals without significant differences compared to the control. K. africana fruit also chelated iron significantly compared to the control. The fruit extract inhibited iron-induced lipid peroxidation in the rat pancreas and ?-amylase activity compared to the control. K. africana fruit displayed promising potential in inhibiting ?-amylase activity and associated lipid peroxidation in diabetics. Therefore, it holds strong promise for use in diabetes treatment, validating its traditional use for managing the condition.

EFFECT OF WHITE SUGAR, BROWN SUGAR AND JAGGERY POWDER SYRUP ON BIOCHEMICAL AND HISTOPATHOLOGICAL MARKERS OF SPRAGUE-DAWLEY RATS

Hypertension accounts for 10% of the total annual health budget in developed countries.1 By 2025, the number of people living with hypertension is expected to reach 1.56 billion people.2Dietary factors that increase blood pressure (BP) are of interest to public health authorities.3,4Twenty adult male Sprague-Dawley rats were taken. All groups received standard chow ad libitum. Controls (A), received plain drinking water, and the Sucrose treatment rats received 10% sucrose solution prepared daily for 12 weeks. Non-invasive blood pressure was recorded using computer based data recording system power lab model: M-ML 856, Australia with rat tail cuff attachment.Blood samples were collected. Serum aliquots were frozen at ?80°C for: ALT, AST, TG, total cholesterol (TC), and high-density lipoprotein (HDL) were determined using commercial enzymatic methods (CELM diagnosis, São Paulo, Brazil). The concentration of VLDL and low-density lipoprotein was measured. ANOVA and Post-Hoc Tukey tests were applied to determine statistical difference among the study groups. The results showed variable effects on biochemical and histopathological findings in rat liver, kidney and pancreas. The pancreas and kidneys of the rats showed adverse inflammatory histopathological changes maximally in rats taking jaggery syrup (Shakkar) flowed by white sugar and minimal in Shakkar. The adverse effects on liver cells were maximally seen on rats given brown sugar. This study enabled us to better understand the biochemical and histopathological effects of various types of sugars available in Pakistani market in order to create awareness regarding their effects on health.

Effects of Insulin and Resveratrol Versus Mesenchymal Stem Cells (MSCs) on the pancreas of Diabetic Rats (Type-I) (Light and Electron Microscope Study)

Effects of Insulin and Resveratrol Versus Mesenchymal Stem Cells (MSCs) on the pancreas of Diabetic Rats (Type-I) (Light and Electron Microscope Study)

The Protective Effects of Vanillic Acid and Vanillic Acid-Coated Silver Nanoparticles (AgNPs) in Streptozotocin-Induced Diabetic Rats.

The production of nanoparticles enhances the bioactivity of biological molecules for drug delivery to diseased sites. This study explains how silver nanoparticle (AgNP) coating enhanced the protection effects of vanillic acid in male diabetic rats with streptozotocin- (STZ-) induced diabetes. Twenty-four rats were divided into four groups (n = 6) for this investigation. The first group (G1) is untreated, whereas diabetes was induced in the other three groups through STZ injection. Diabetic rats that were not getting therapy were included in the second group (G2, STZ-positive), whereas the other diabetic rats were divided into the third group (G3, vanillic acid-treated) and the fourth group (G4, vanillic acid-coated AgNPs treated). The treatment lasted four weeks. In G2, the induction of diabetes significantly (at P = 0.05) increased in serum glucose, glycated proteins, renal indices, interleukin-6 (IL-6), K+, immunoglobulins, and lipid peroxidation, while decreased Ca++, Na+, and other antioxidants in the kidney tissue homogenate. In addition, pathological altered signs were present in the pancreas and kidneys of diabetic rats. The renal and pancreatic tissues were effectively enhanced by vanillic acid or vanillic acid-coated AgNPs, bringing them very close to their prediabetic conditions. Vanillic acid-coated AgNPs offered a stronger defense against STZ-induced diabetes and lessened the effects of hyperglycemia compared to ordinary vanillic acid. Additionally, using vanillic acid coated with silver nanoparticles greatly increased the antioxidant and antidiabetic activity and reduced inflammation when compared to using vanillic acid alone.

Optimization of the selection of the volume of surgical intervention in cases of pronounced morphological and structural changes of the parenchyma in patients with a high risk of developing pancreatic cancer

Chronic pancreatitis is a common recurrent pathology of the pancreas. The long course of the inflammatory process, accompanied by chronicity, is often attributed to the causes that lead to the development of pancreatic cancer. The aim of the work is to study the morphological changes of the pancreas in rats and the level of matrix metalloproteinases and tissue inhibitor of metalloproteinases in patients with complicated forms of chronic pancreatitis and a high risk of developing pancreatic cancer in order to optimize the selection of the volume of surgical intervention. A histological study of the pancreas of rats with chronic pancreatitis and chronic pancreatitis on the background of diabetes was carried out. 27 patients operated on during 2020-2022 were examined. In 15 of them, we were unable to clearly and convincingly differentiate of chronic pancreatitis from pancreatic cancer, since quite often the clinical symptoms and diagnostic picture of these diseases are similar. In the remaining 12 patients it was confirmed with all the inherent clinical signs of chronic pancreatitis and ductal hypertension. Matrix metalloproteinases (MMP-1, -2, -3, -8, -9, -10) and tissue inhibitor of metalloproteinases were studied. The obtained results were processed statistically. Morphological changes of the pancreas in rats correspond to high and moderate ductal dysplasia of the PanIN 2 and PanIN 3 class, which are direct predictors of pancreatic adenocarcinoma. In 22 patients moderate and severe exocrine insufficiency was observed, confirmed by a significant decrease in fecal elastase. An intraoperative biopsy of the changed tissue of the pancreas was performed. Among the 15 operated patients of the main group, 9 were diagnosed with diabetes mellitus and changes in MMTs and a peptide pool inherent in malignant tissue. Intraoperatively, after performing a punch biopsy, acinar metaplasia was detected in 3 patients, tissue changes characteristic of PanIN2-PanIN3 in 4 patients, and pancreatic cancer in the head area was confirmed in 3 patients. Changes in the protein profile of the plasma, clinical manifestations, as well as characteristic changes in the pancreas tissue, gave us grounds for performing extended resection interventions. Studying the morphological structure of the pancreas, using as many methods as possible for differential diagnosis between chronic pancreatitis and pancreatic cancer, as well as a comprehensive approach to the patient will allow for the most correct and effective intervention.

Antidiabetic Activity of Ethanol-Water Fraction of Longjack Root (Eurycoma longifolia Jack.) in Streptozotocin-Nicotinamide Induced Rats

This study aims to determine the decrease in glucose levels, MDA levels, and histopathological appearance of the pancreatic organs of Wistar white rats after administration of the ethanol-water fraction of longjack root. This study used a completely randomized design with four treatment groups and six replications. The treatment consisted of normal control, negative control (Na-CMC 0.5% 5 ml/200 g body weight), positive control (glibenclamide 0.09 mg/200 g body weight), and treatment of the ethanol-water fraction of longjack root with a dose of 500 mg/kg body weight. The results showed that the ethanol-water fraction of longjack root at a dose of 500 mg/kg body weight had antidiabetic activity comparable to that of glibenclamide at a dose of 0.09/200 g body weight, namely blood glucose levels and MDA levels in white rats of 123.55 mg/dl and 2.83 nmol/ml. The results of histopathological analysis of the pancreas of white rats showed that administration of the ethanol-water fraction of longjack root could repair damage to the islets of Langerhans due to the administration of streptozotocin-nicotinamide.

Serotonin transporter imaging agent as a probe for β-cells of pancreas

ObjectiveDiabetes mellitus (DM) is one of the major diseases in the world. Nuclear medicine imaging may be able to detect functional status of pancreatic β cells in vivo, which might elucidate the pathological mechanisms of diabetes and develop individualized treatment plans. In this study, we evaluated the ability of [125I]ADAM, a serotonin transporter (SERT) imaging agent, as a probe for detecting pancreatic β-cell mass (BCM). MethodsIn vitro cell studies were evaluated in INS-1 cells (rat islet β cell line). Biodistribution studies were performed in male normal Sprague-Dawley rats and alloxan-induced type 1 diabetes mellitus (T1DM) rats. Distribution and expression of SERT protein in pancreas of rats were also measured by immunofluorescence staining and Western blot. ResultsIn vitro cell studies showed that the concentration of [125I]ADAM associated with the INS-1 cells was increased gradually with incubation time, and the SERT specific inhibitor, escitalopram, exhibited the inhibitory effect on this interaction. Biodistribution studies also showed that the uptake of [125I]ADAM in the pancreas of normal rats was decreased in the presence of escitalopram. However, in the T1DM rat model with a significant β cells reduction, the uptake of pancreas was increased when compared with the control. Through immunofluorescence staining and Western blot, it was found that both the endocrine and exocrine cells of the normal pancreas expressed SERT protein, and the level of SERT protein in the exocrine cells was higher than islets. In the diabetic state, the expression of SERT in the exocrine cells was further increased. ConclusionsThe SERT imaging agent, [125I]ADAM, at the present form will not be suitable for imaging β cells, specifically because there were extraordinarily high non-specific signals contributing from the exocrine cells of pancreas. In addition, we noticed that the level of SERT expression was abnormally elevated in the diabetic state, which might provide an unexpected target for studying the pathological mechanisms of diabetes.

New Fluorescent Dye for the Detection of Zn2+ in Living Cells and Fixed Sections of the Rat Pancreas.

We report the synthesis and characterization of a new 4-methoxyphenyl-2,2'-bipyridine-based ligand, such as 12, bearing dipicolylaminomethyl core as a receptor unit, as a probe for the fluorescence "turn-on" detection of Zn2+. Thus, in the presence of Zn2+ the probe 12 exhibited a fluorescence enhancement with a Stokes shift of ~ 180nm and photoluminescence quantum yields value of ~ 1.0. In addition, 12 exhibited higher binding constant for Zn2+ (~ 2 × 105M-1) with the LOD reaching the nanomolar level (~ 0.1 × 10-9M) compare to the previously reported probe 1. The stoichiometry and structure of the [Zn(12)]2+ and [Zn(1)]2+ complexes were supported by XRD analysis, DFT calculations and 1H NMR experiments. It was postulated that, as a result of binding of Zn2+, the sample exhibited a bright "on" state via the PET-ICT processes. Molecular docking studies and confocal fluorescence microscopy experiments demonstrated that the probe 12 could be used for the fluorescence detection of Zn2+ not only in artificially enriched with zinc salts live cells, but also in fixed tissues with cations are in a bound state. The high binding constant of compound 12 to Zn2+ cation allows it to be used for the accurate localization of pancreatic beta cells (islets of Langerhans).

L-tryptophan effectively prevents fatty degeneration of rat pancreas

Alimentary obesity is a risk factor for the development of many pathophysiological conditions in various organs, including the pancreas. Thus, the study of mechanisms, clinical symptoms and ways to prevent the development of fatty degeneration of pancreas at obesity is a current direction of research. The aim of our work was to study the influence of L-tryptophan on the morphofunctional changes of the pancreas of rats with diet-induced obesity and to evaluate the possibility of its use for the prevention of the development of the gland fatty degeneration. The study was conducted in male Wistar rats, which were 3 months old at the experiment beginning. Histologic preparations were made from pancreas tissue samples using a standard method. Morphometric measurements were performed on digital images using “Image J” software. In biochemical studies, we determined concentration of glucose in blood serum and of triglycerides, lipids and cholesterol in pancreas tissue samples. It was found that rats fed a high-fat, high-carbohydrate diet showed marked sings of developing alimentary obesity. This was evidenced by a significant increase in the weight of visceral fat (by 147%) and obesity index (by 129%). The exposure of rats to a high-calorie diet resulted in the emergence of distinct signs indicating hypofunction in both the exocrine and, to a greater extent, endocrine sections of the pancreas. The administration of L-tryptophan reduced the intensity of accumulation of visceral fat and fat in the gland itself. This was evidenced by lower concentrations of lipids (by 53%) and triglycerides (by 32%) in the pancreatic tissue compared to high-calorie diet rats. In addition, L-tryptophan prevented an excessive decrease in the function of both the exocrine and endocrine parts of the gland from the harmful effects of dietary obesity. This may be of practical interest when using tryptophan and its derivatives in the clinic to prevent a decrease in gland activity in this pathology.

Evaluating the Biocompatibility of Decellularized Pancreas and Its Histological Features as a Support Structure for Adipose Mesenchymal Stem Cell Culture

Background: Tissue engineering is a multidisciplinary and interdisciplinary topic that involves the development of biological implants for tissue regeneration intending to improve or enhance tissue or organ function. Objectives: This study aimed to evaluate the mechanical and histological properties of decellularized rat pancreas scaffolds, as well as to investigate the viability of adipose mesenchymal stem cells (MSCs) on the said scaffold for use in regenerative medicine and tissue engineering. Methods: This is an experimental study that was performed in the research laboratory of Mohaghegh Ardabili University. To prepare the scaffold, male Wistar rats were anesthetized with carbon dioxide. After dissecting the mice, their pancreases were isolated and immediately transferred to a phosphate-buffered saline (PBS) solution to prepare them for decellularization. The decellularized scaffolds were evaluated histologically and mechanically. After decellularization, lipid MSCs were injected into de-cell scaffolds in the third passage. Results: Examination of the results of histological evaluations showed that scaffolding was completely decellularized. These results were confirmed by Mason trichrome and Dapi staining (coloring). Specialized tissue assessments by electron microscopy showed that the collagen and elastin strands were relatively conserved in the extracellular matrix (ECM). Conclusions: In general, the result of this research demonstrates the successful decellularization of pancreatic tissue, effective preservation of the ECM of the desired tissue, and the viability of the MSCs on the scaffold resulting from the decellularization of the tissue.