scholarly journals Panax notoginseng Promotes Repair of Colonic Microvascular Injury in Sprague-Dawley Rats with Experimental Colitis

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Shiying Wang ◽  
Ping Tao ◽  
Lei Zhao ◽  
Wangjun Zhang ◽  
Hongyi Hu ◽  
...  
Keyword(s):  
Colonic Mucosa ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Panax Notoginseng ◽  
Control Group ◽  
Therapeutic Effects ◽  
Serum Concentrations ◽  
Sprague Dawley ◽  
Microvascular Injury ◽  
Colitis Model

To investigate the therapeutic effects of PN on intestinal inflammation and microvascular injury and its mechanisms, dextran sodium sulfate- (DSS-) or iodoacetamide- (IA-) induced rat colitis models were used. After colitis model was established, PN was orally administered for 7 days at daily dosage of 1.0 g/kg. Obvious colonic inflammation and mucosal injuries and microvessels were observed in DSS- and IA-induced colitis groups. DAI scores, serum concentrations of VEGFA121, VEGFA165, VEGFA165/VEGFA121, IL-6, and TNF-α, and expression of Rap1GAP and TSP1 proteins in the colon were significantly higher while serum concentrations of IL-4 and IL-10 and MVD in colon were significantly lower in the colitis model groups than in the normal control group. PN promoted repair of colonic mucosal injury and microvessels, attenuated inflammation, and decreased DAI scores in rats with colitis. PN also decreased the serum concentrations of VEGFA121, VEGFA165, VEGFA165/VEGFA121, IL-6, and TNF-α and increased the serum concentrations of IL-4 and IL-10, with the expression of Rap1GAP and TSP1 proteins in colonic mucosa being downregulated. The constituents of PN were identified with HPLC-DAD. To sum up, PN could promote repair of injuries of colonic mucosa and microvessels via downregulating VEGFA isoforms and inhibiting Rap1GAP/TSP1 signaling pathway.

Chylomicrons-Simulating Sustained Drug Release in Mesenteric Lymphatics for the Treatment of Crohn’s-Like Colitis

2020 ◽  
Author(s):  
Yi Yin ◽  
Jingjing Yang ◽  
Yongchun Pan ◽  
Zhen Guo ◽  
Yanfeng Gao ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Drug Release ◽  
Drug Delivery System ◽  
Delivery System ◽  
Lymphatic System ◽  
Intestinal Inflammation ◽  
Lymphatic Vessels ◽  
Experimental Colitis ◽  
Therapeutic Effects ◽  
Sustained Drug Release

Abstract Background and Aims Alteration to both the structures and functions of mesenteric lymphatic vessels is a typical hallmark of Crohn’s disease [CD]. Dysfunctional lymphatics was observed in patients with both CD and experimental colitis, suggesting mesenteric lymphatics could be potential therapeutic targets. This study aimed to develop a nano-delivery system which can enhance drug delivery in mesenteric lymphatic tissue [MLT] and evaluate the therapeutic effects in Crohn’s colitis. Methods We designed a mesoporous silica nanoparticle [MSN] conjugated with long-chain fatty acid [LMSN] and covered with enteric coating [ELMSN] which can be specifically transported via the mesenteric lymphatic system. The therapeutic efficacy of laquinimod-loaded nanoparticles [LAQ@ELMSN] was evaluated in the well-established interleukin [IL]-10−/− spontaneous experimental colitis. Results ELMSNs induced sustainable drug release that markedly increased drug concentration in MLT. In experimental colitis, the lymphatics-targeting drug delivery system suppressed lymphangitis and promoted lymphatic drainage. The downregulation of pro-inflammatory cytokines and the downstream NF-κB-related proteins efficiently inhibited lymphangiogenesis and restored tight junctions of mesenteric lymphatic vessels [MLVs]. LAQ@ELMSN showed a superior therapeutic effect in ameliorating intestinal inflammation compared with free drug administration. Alteration of gut microbiota and metabolites in experimental colitis was also reversed by LAQ@ELMSN. Conclusion Our study demonstrates a convenient, orally administered drug delivery system which enhances drug release in MLT. The results confirm the contribution of the mesenteric lymphatic system to the pathogenesis of gut inflammation and shed light on the application of lymphatics-targeting drug delivery therapy as a potential therapeutic strategy for CD treatment.

scholarly journals Sulodexide Protects Contrast-Induced Nephropathy in Sprague-Dawley Rats

2016 ◽  
Vol 40 (3-4) ◽  
pp. 621-632 ◽  
Author(s):  
Qing Zhao ◽  
Jianyong Yin ◽  
Zeyuan Lu ◽  
Yiwei Kong ◽  
Guangyuan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Vehicle Group ◽  
Control Group ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Contrast Induced Nephropathy ◽  
Sprague Dawley Rats ◽  
Hk2 Cells

Background: Sulodexide is a powerful antithrombin agent with reno-protective property. However, whether it has beneficial effects on Contrast-Induced Nephropathy (CIN) remained elusive. In the current study, we evaluated the therapeutic effects of Sulodexide on CIN and investigated the potential mechanisms. Methods: CIN model was induced by intravenous injection of indomethacin, followed by Ioversol and L-NAME. Sprague-Dawley rats were divided into 4 groups: control group, CIN group, CIN+vehicle group (CIN rats pretreated with vehicle) and CIN+ Sulodexide (CIN rats pretreated with Sulodexide). Sulodexide or an equivalent volume of vehicle was intravenously delivered 30 min before the induction of CIN. All the animals were sacrificed at 24h after CIN and tissues were harvested to evaluate renal injury, kidney oxidative stress and apoptosis levels. Plasma antithrombin III (ATIII) activities were also measured. Results: Compared to the untreated CIN group, improved renal function, reduced tubular injury, decreased levels of oxidative stress and apoptosis were observed in CIN rats receiving Sulodexide injection. In addition, we also found that ATIII activity was significantly higher in Sulodexide-administered group than that in vehicle-injected CIN rats. For in vitro studies, HK2 cells were exposed to Ioversol and the cyto-protective effects of Sulodexide were also determined. Sulodexide pretreatment protected HK2 cells against the cytotoxicity of Ioversol via inhibiting caspase-3 activity. Preincubation with Sulodexide could also attenuate H2O2-induced increases in ROS, apoptosis and caspase-3 levels. Conclusions: Taken together, Sulodexide could protect against CIN through activating ATIII, and inhibiting oxidative stress, inflammation and apoptosis.

Effect of Electro-acupuncture on Ultrastructure in Diabetic Gastroparesis Model Rats

2015 ◽  
Vol 3 (1) ◽  
pp. 70-76
Author(s):  
Feng-E He ◽  
Quan-Quan Wan ◽  
Yan Peng ◽  
Ya-Ping Lin ◽  
Jing Shen
Keyword(s):  
Smooth Muscle ◽  
Point Group ◽  
Diabetic Gastroparesis ◽  
Control Group ◽  
Therapeutic Effects ◽  
Phenol Red ◽  
Model Group ◽  
Sprague Dawley ◽  
Blank Control Group ◽  
Gastric Emptying Rate

Abstract Objective: To observe the effects of electro-acupuncture (EA) on ultrastructure of gastric antrum smooth muscle cells (GASMCs) in diabetic gastroparesis (DGP) model rats, and to explore the possible mechanism underlying the therapeutic effects of EA. Methods: Sixty Sprague Dawley rats were randomly divided into 5 groups: blank control (group A), DGP model (group B), EA point (group C), EA non-point (group D), Metoclopramide control (group E). DGP rat model was established by 2% STZ intraperitoneal injection at once, and then being fed with high-sugar-high-fat (HSHF) for 8wks. Phenol red lavage method was employed to measure gastric emptying rate (GER) and intestinal migration rate (IMR). The ultrastructure of GASMCs was observed under the electronic microscope. Results: Compared with the blank control group, the GER and IMR in model group were decreased significantly (P＜0.05 or P＜0.01). Compared with the model group, the GER and IMR in EA point group were increased significantly(P＜0.05 or P＜0.01). Electro-acupuncture on “Zu San Li”(ST36) point, etc. has been observed improving the ultrastructure of GASMCs, as well as increasing the number of interstitial cells of Cajal (ICCs). Conclusion: Electro-acupuncture can improve the GI motility promisingly, based on a potential underlying mechanism that the electro-acupuncture can improve the ultrastructure of gastric smooth muscle, and increase the number of ICCs.

scholarly journals Effects of budesonide and probiotics enemas on the colonic mucosa of rats with experimental colitis

2007 ◽  
Vol 22 (1) ◽  
pp. 34-38
Author(s):  
Mardem Machado de Souza ◽  
José Eduardo de Aguilar-Nascimento ◽  
Maria Helena Gomes-da-Silva ◽  
Rubens Carlos Junior
Keyword(s):  
Dna Content ◽  
Colonic Mucosa ◽  
Experimental Colitis ◽  
Control Group ◽  
Group 4 ◽  
Histological Score ◽  
Significant Difference ◽  
Male Wistar Rats ◽  
Group 5 ◽  
Group 2

PURPOSE: To investigate the effect of enemas containing probiotics and budesonide on the colonic mucosa in experimental colitis. METHODS: Fifty male Wistar rats with experimental colitis induced by 10% acetic acid enema were randomized to five groups (10 rats each) according to the treatment: group 1 - saline solution, group 2 - budesonide (0.75 mg/kg/day), group 3 - probiotics (1mg/day), group 4 - probiotics plus budesonide, and group 5 - control, with not-treated rats. The following variables were studied: body weight, macroscopic and microscopic score of the colonic mucosa, and DNA content of the mucosa. RESULTS: All animals lost weight between the beginning and the end of the experiment (280+ 16 mg versus 249+21 mg, p< 0.001). There was no significant difference among the groups in relation to both the macroscopic and histological score. The budesonide + probiotic group showed higher DNA content than control group (1.24+ 0.15 versus 0.92+ 0.30 mg/100mg of tissue, p=0.01). CONCLUSION: Budesonide in addition to probiotics enhance the mucosal trophism in experimental colitis.

scholarly journals Effects of initiating time and dosage of Panax notoginseng on mucosal microvascular injury in experimental colitis

2017 ◽  
Vol 23 (47) ◽  
pp. 8308-8320 ◽  
Author(s):  
Shi-Ying Wang ◽  
Ping Tao ◽  
Hong-Yi Hu ◽  
Jian-Ye Yuan ◽  
Lei Zhao ◽  
...  
Keyword(s):  
Experimental Colitis ◽  
Panax Notoginseng ◽  
Microvascular Injury

scholarly journals Hyaluronan Synthase 3 Null Mice Exhibit Decreased Intestinal Inflammation and Tissue Damage in the DSS-Induced Colitis Model

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Sean P. Kessler ◽  
Dana R. Obery ◽  
Carol de la Motte
Keyword(s):  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Experimental Colitis ◽  
Hyaluronan Synthase ◽  
Wild Type ◽  
Colon Tissue ◽  
Dss Colitis ◽  
Chemically Induced ◽  
Inflammatory Bowel ◽  
Colitis Model

Hyaluronan (HA) overproduction is a hallmark of multiple inflammatory diseases, including inflammatory bowel disease (IBD). Hyaluronan can act as a leukocyte recruitment molecule and in the most common mouse model of intestinal inflammation, the chemically induced dextran sodium sulfate (DSS) experimental colitis model, we previously determined that changes in colon distribution of HA occur before inflammation. Therefore, we hypothesized that, during a pathologic challenge, HA promotes inflammation. In this study, we tested the progression of inflammation in mice null for the hyaluronan synthase genes (HAS1, HAS3, or both HAS1 and HAS3) in the DSS-colitis model. Our data demonstrate that both the HAS1/HAS3 double and the HAS3 null mice are protected from colitis, compared to wild-type and HAS1 null mice, as determined by measurement of weight loss, disease activity, serum IL-6 levels, histologic scoring, and immunohistochemistry. Most notable is the dramatic increase in submucosal microvasculature, hyaluronan deposition, and leukocyte infiltration in the inflamed colon tissue of wild-type and HAS1 null mice. Our data suggest, HAS3 plays a crucial role in driving gut inflammation. Developing a temporary targeted therapeutic intervention of HAS3 expression or function in the microcirculation may emerge as a desirable strategy toward tempering colitis in patients undergoing flares of IBD.

Electroacupuncture Protects against Articular Cartilage Erosion by Inhibiting Mitogen-Activated Protein Kinases in a Rat Model of Osteoarthritis

2016 ◽  
Vol 34 (4) ◽  
pp. 290-295 ◽  
Author(s):  
Ying Liao ◽  
Xinhong Li ◽  
Neng Li ◽  
Jun Zhou
Keyword(s):  
Articular Cartilage ◽  
Protein Kinases ◽  
Cruciate Ligament ◽  
Control Group ◽  
Therapeutic Effects ◽  
Sprague Dawley ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Cartilage Erosion ◽  
Group Control Group

Objective The therapeutic effects of electroacupuncture (EA) on osteoarthritis (OA) are well documented; however, the precise mechanisms of action have not yet been fully elucidated. The present study aimed to investigate the effect of EA on cartilage in an experimental animal model of OA induced by anterior cruciate ligament transection (ACLT) and to examine for concomitant changes in the expression of mitogen-activated protein kinases (MAPKs) in the articular cartilage. Methods Thirty-three-month-old male Sprague Dawley rats were randomly divided into the following three groups (n=10 each): sham operated group (Control group), ACLT without treatment (ACLT group), and ACLT with EA treatment (ACLT+EA group). One week after ACLT, rats in the ACLT+EA group received 12 weeks of EA treatment. Histological analysis and quantitative real-time PCR were used to investigate the effects of EA on cartilage morphology (quantified using modified Mankin scores) and expression of MAPKs (p38, c-Jun N-terminal kinase (c-Jun), and extracellular signal-regulated kinase (ERK)1), respectively. Results ACLT produced coarse cartilage surfaces, fibrous degeneration, and fissuring, all of which were suppressed by EA treatment. Although Mankin scores in the ACLT+EA group were significantly higher compared to the Control group (p<0.01), they were significantly lower than the (untreated) ACLT group (p<0.01). The increase in mRNA expression of p38, c-Jun, ERK1, and matrix metalloproteinase (MMP)-13 observed in cartilage after ACLT was significantly inhibited by EA. Conclusions EA appears to prevent the degeneration of articular cartilage, at least partly through regulation of MMP-13 and inhibition of MAPKs in the cartilage of rats with ACLT-induced OA.

Topographical Changes of Rat's Colonic Mucosal After Chronic Arsenic Exposure - A Scanning Electron Microscopy Study

2018 ◽  
Vol 17 (1) ◽  
Author(s):  
Khodijah Zulkiflee ◽  
Zunariah Buyong ◽  
Asmah Hanim Hamdan ◽  
Shahida Saharudin ◽  
Wan Muhamad Salahudin Wan Salleh
Keyword(s):  
Colonic Mucosa ◽  
Arsenic Exposure ◽  
Goblet Cells ◽  
Microscopy Study ◽  
Control Group ◽  
Sprague Dawley ◽  
Uniform Size ◽  
Sprague Dawley Rats ◽  
Organic Arsenic ◽  
Scanning Electron

Introduction: Human are exposed to arsenic threats in several ways. Our drinking water for instance, can be hazardous due to the contamination of arsenic-based pesticide and herbicide into our water supply. The most vulnerable part of our body due to ingestion of arsenic is our gastrointestinal system. Thus, the aim of this study was to determine the effects of chronic exposure to organic arsenic (Monosodium methylarsonate, MSMA) on the surface topography of rat's colonic mucosa by using scanning electron microscope (SEM). Materials and Methods: 30 Sprague Dawley rats were given daily oral gavage of MSMA 42.13 mg/kg, which is 1/30 LD50, and 30 Sprague Dawley rats acted as control. 10 exposed rats and 10 control rats were sacrificed at regular intervals (2 months, 4 months and 6 months) and their colon specimens were examined by SEM. Results: In the control group, the colonic mucosa appeared normal with uniform size individual glandular units and has a central crypt orifice. The goblet cells were located in between the absorptive cells to produce mucous. In the exposed group, the rat's colonic mucosa showed increasing features of surface alterations such as haphazard shape of glandular units, slit-like crypt opening and less goblet cells with reduced number of microvilli. Conclusion: There were topographical changes of colonic mucosa of rats exposed to chronic low dose of organic arsenic.

scholarly journals Peritoneal Air Exposure Elicits an Intestinal Inflammation Resulting in Postoperative Ileus

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Shanjun Tan ◽  
Wenkui Yu ◽  
Zhiliang Lin ◽  
Qiyi Chen ◽  
Jialiang Shi ◽  
...  
Keyword(s):  
Postoperative Ileus ◽  
Intestinal Inflammation ◽  
Gastrointestinal Transit ◽  
Serum Levels ◽  
Underlying Mechanism ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Sprague Dawley ◽  
Air Exposure ◽  
Total Antioxidant

Background.The pathogenesis of postoperative ileus (POI) is complex. The present study was designed to investigate the effects of peritoneal air exposure on the POI intestinal inflammation and the underlying mechanism.Methods.Sprague-Dawley rats were randomized into five groups (6/group): the control group, the sham group, and three exposure groups with peritoneal air exposure for 1, 2, or 3 h. At 24 h after surgery, we analyzed the gastrointestinal transit, the serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10, the myeloperoxidase activity, and the levels of TNF-α, IL-1β, IL-6, and IL-10 in the ileum and colon. The oxidant and antioxidant levels in the ileum and colon were analyzed by measuring malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC).Results.Peritoneal air exposure caused an air-exposure-time-dependent decrease in the gastrointestinal transit. The length of peritoneal air exposure is correlated with the severity of both systemic and intestinal inflammations and the increases in the levels of MDA, SOD, GSH-Px, and T-AOC.Conclusions.The length of peritoneal air exposure is proportional to the degree of intestinal paralysis and the severity of intestinal inflammation, which is linked to the oxidative stress response.

scholarly journals Si Shen Wan Regulates Phospholipase Cγ-1 and PI3K/Akt Signal in Colonic Mucosa from Rats with Colitis

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Duan-yong Liu ◽  
Rong Xu ◽  
Min-fang Huang ◽  
Hong-yan Huang ◽  
Xin Wang ◽  
...  
Keyword(s):  
Sulfonic Acid ◽  
Colonic Mucosa ◽  
Intestinal Epithelial Cells ◽  
Experimental Colitis ◽  
Mucosal Injury ◽  
Signal Pathway ◽  
Trinitrobenzene Sulfonic Acid ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

The present study explored the feasible pathway of Si Shen Wan (SSW) in inhibiting apoptosis of intestinal epithelial cells (IECs) by observing activation of phospholipase Cγ-1 (PLC-γ1) and PI3K/Akt signal in colonic mucosa from rats with colitis. Experimental colitis was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in the Sprague-Dawley rats. After SSW was administrated for 7 days after TNBS infusion, western blot showed an increment in levels of PI3K, p-Akt, and IL-23 and a decrement in levels of PLC-γ1 and HSP70 in colonic mucosal injury induced by TNBS. Meanwhile, assessments by ELISA revealed an increment in concentrations of IL-2, IL-6, and IL-17 and a reduction in level of TGF-βafter TNBS challenge. Impressively, treatment with SSW for 7 days significantly attenuated the expressions of PI3K and p-Akt and the secretion of IL-2, IL-6, IL-17, and IL-23 and promoted the activation of PLC-γ1, HSP70, and TGF-β. Our previous studies had demonstrated that SSW restored colonic mucosal ulcers by inhibiting apoptosis of IECs. The present study demonstrated that the effect of SSW on inhibiting apoptosis of IECs was realized probably by activation of PLC-γ1 and suppression of PI3K/Akt signal pathway.

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