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| 1 | Esophagogastric anastomosis in rats: Improved healing by BPC 157 and L-arginine, aggravated by L-NAME显示文摘AIM To cure typically life-threatening esophagogastric anastomosis in rats, lacking anastomosis healing and sphincter function rescue, in particular. METHODS Because we assume esophagogastric fistulas represent a particular NO-system disability, we attempt to identify the benefits of anti-ulcer stable gastric pentadecapeptide BPC 157, which was in trials for ulcerative colitis and currently for multiple sclerosis, in rats with esophagocutaneous fistulas. Previously, BPC 157 therapies have promoted the healing of intestinal anastomosis and fistulas, and esophagitis and gastric lesions, along with rescued sphincter function. Additionally, BPC 157 particularly interacts with the NOsystem. In the 4 d after esophagogastric anastomosis creation, rats received medication(/kg intraperitoneallyonce daily: BPC 157(10 μg, 10 ng), L-NAME(5 mg), or L-arginine(100 mg) alone and/or combined or BPC 157(10 μg, 10 ng) in drinking water). For rats underwent esophagogastric anastomosis, daily assessment included progressive stomach damage(sum of the longest diameters, mm), esophagitis(scored 0-5), weak anastomosis(m L H2 O before leak), low pressure in esophagus at anastomosis and in the pyloric sphincter(cm H2O), progressive weight loss(g) and mortality. Immediate effect assessed blood vessels disappearance(scored 0-5) at the stomach surface immediately after anastomosis creation. RESULTS BPC 157(all regimens) fully counteracted the perilous disease course from the very beginning(i.e., with the BPC 157 bath, blood vessels remained present at the gastric surface after anastomosis creation) and eliminated mortality. Additionally, BPC 157 treatment in combination with L-NAME nullified any effect of L-NAME that otherwise intensified the regular course. Consistently, with worsening(with L-NAME administration) and amelioration(with L-arginine), either L-arginine amelioration prevails(attenuated esophageal and gastric lesions) or they counteract each other(L-NAME + L-arginine); with the addition of BPC 157(L-NAME + L-arginine + BPC 157), there was a marked beneficial effect. BPC 157 treatment for esophagogastric anastomosis, along with NOS-blocker L-NAME and/or NOS substrate L-arginine, demonstrated an innate NO-system disability(as observed with L-arginine effectiveness). BPC 157 distinctively affected corresponding events: worsening(obtained with L-NAME administration that was counteracted); or amelioration(L-arginine + BPC 157-rats correspond to BPC 157-rats).CONCLUSION Innate NO-system disability for esophagogastric anastomoses, including L-NAME-worsening, suggests that these effects could be corrected by L-arginine and almost completely eliminated by BPC 157 therapy. | Zeljko Djakovic Ivka Djakovic Vedran Cesarec Goran Madzarac Tomislav Becejac Goran Zukanovic Domagoj Drmic Lovorka Batelja Anita Zenko Sever Danijela Kolenc Alen Pajtak Nikica Knez Mladen Japjec Kresimir Luetic Dinko Stancic-Rokotov Sven Seiwerth Predrag Sikiric | 2016 | World Journal of Gastroenterology2016，22，41： | 3 |
| 2 | Pentadecapeptide BPC 157 resolves suprahepatic occlusion of the inferior caval vein, Budd-Chiari syndrome model in ratsPentadecapeptide BPC 157 resolves suprahepatic occlusion of the inferior caval vein, Budd-Chiari syndrome model in rats显示文摘BACKGROUND Recently,as a possible therapy resolving solution,pentadecapeptide BPC 157 therapy,has been used in alleviating various vascular occlusion disturbances.BPC 157 was previously reviewed as novel mediator of Robert cytoprotection and endothelium protection in the stomach,and gut-brain axis,beneficial therapy in gastrointestinal tract,with particular reference to vascular recruitment,ulcerative colitis and tumor cachexia,and other tissues healing.Here we raised new hypothesis about BPC 157 therapy in the Budd-Chiari syndrome in rats,rapid bypassing of the suprahepatic inferior caval vein occlusion,and rats recovery with the active and effective pharmacotherapy treatment.AIM To investigate Budd-Chiari syndrome model(inferior caval vein suprahepatic occlusion)resolution,since BPC 157 resolves various rat vascular occlusion.METHODS We assessed the activated bypassing pathways between the inferior and superior caval veins and portocaval shunt,counteracted caval/portal hypertension,aortal hypotension,venous/arterial thrombosis,electrocardiogram disturbances,liver and gastrointestinal lesions(i.e.,stomach and duodenum hemorrhages,in particular,congestion).Rats with suprahepatic occlusion of the inferior vena cava by ligation were medicated at 1 min,15 min,24 h,or 48 h post-ligation.Medication consisted of 10μg/kg BPC 157,10 ng BPC 157 or 5 m L/kg saline,administered once as an abdominal bath or intragastric application.Gross and microscopic observations were made,in addition to assessments of electrical activity of the heart(electrocardiogram),portal and caval hypertension,aortal hypotension,thrombosis,hepatomegaly,splenomegaly and venography.Furthermore,levels of nitric oxide,malondialdehyde in the liver and serum enzymes were determined.RESULTS BPC 157 counteracted increased P wave amplitude,tachycardia and ST-elevation,i.e.,right heart failure from acute thrombotic coronary occlusion.The bypassing pathway of the inferior vena cava-azygos(hemiazygos)vein-superior vena cava and portocaval shunt occurred rapidly.Even with severe caval portal hypertension,BPC 157 antagonized portal and caval hypertension and aortal hypotension,and also reduced refractory ascites.Thrombosis of portal vein tributaries,inferior vena cava,and hepatic and coronary arteries was attenuated.In addition,there was reduced pathology of the lungs(severe capillary congestion)and liver(dilated central veins and terminal portal venules),decreased intestine hemorrhagic lesions(substantial capillary congestion,submucosal edema and architecture loss),and increased liver and spleen weight.During the period of ligation,nitric oxide-and malondialdehyde-levels in the liver remained within normal healthy values,and increases in serum enzymes were markedly reduced.CONCLUSION BPC 157 counteracts Budd Chiari syndrome in rats. | Slaven Gojkovic Ivan Krezic Borna Vrdoljak Dominik Malekinusic Ivan Barisic andreja Petrovic Katarina Horvat Pavlov Marijan Kolovrat Antonija Duzel Mario Knezevic Katarina Kasnik Kovac Domagoj Drmic Lovorka Batelja Vuletic Antonio Kokot Alenka Boban Blagaic Sven Seiwerth Predrag Sikiric | 2020 | World Journal of Gastrointestinal Pathophysiology2020，11，1： | 2 |
| 3 | Advanced glycation endproducts in peripheral nerve in type 2 diabetes with neuropathy显示文摘 | I. Mi?ur K. ?arkovi? A. Barada L. Batelja Z. Mili?evi? Z. Turk | 2004 | Acta Diabetologica2004，，4： | 1 |
| 4 | Anatomical Study of the Facial Nerve Canal in Comparison to the Site of the Lesion in Bell’s Palsy显示文摘 | Krsto Dawidowsky Sre?ko Branica Lovorka Batelja Barbara Dawidowsky Lana Kova?-Bili? Anamarija ?imuni?-Veseli? | 2011 | Collegium Antropologicum2011，，1： | 1 |
| 5 | Bowel adhesion and therapy with the stable gastric pentadecapeptide BPC 157,L-NAME and L-arginine in rats显示文摘BACKGROUND After parietal peritoneum excision with an underlying superficial layer of muscle tissue in rats,there is failed vasculature,and finally,increased adhesion formation.We hypothesized that unlike nitric oxide(NO)-agents,L-NAME and/or L-arginine,the application of the stable gastric pentadecapeptide BPC 157 with its most recent vascular effects(“vascular recruitment”)means attenuated bowel adhesion formation and NO-and malondialdehyde(MDA)-tissue values.AIM To focused on the bowel adhesion and the therapy with the BPC 157,its most and application of NO-agents.METHODS Along with defect creation,medication was(1)during surgery,once,at 1 min after defect creation as an abdominal bath(1 mL/rat),BPC 157(10μg/kg,10 ng/kg,1 mL/rat),an equivolume of saline,L-NAME(5 mg/kg),L-arginine(200 mg/kg)alone and/or combined.Alternatively,medication was(2)intraperitoneally once daily,first application at 30 min after surgery,last application 24 h before assessment at d 7 or d 14.As a postponed therapy to preexisting adhesion(3),BPC 157(10μg/kg,10 ng/kg intraperitoneally,1 mL/rat)was given once daily since d 7.RESULTSThe recovery effect of the BPC 157 regimens goes with the presence of abundant vascular vessels in and near the defect,which occurs rapidly.Lastly,also applied as post-treatment,BPC 157 creates attenuated adhesions,minimal or no adhesion.Contrarily,NO-agents have diverse initial and final effects:The initial weakening of blood vessel disappearance and finally,severe worsening of adhesions(LNAME)vs the initial weakening of blood vessel disappearance and finally,attenuation of adhesions formation(L-arginine),which counteract each other response given together.Importantly,BPC 157 maintains its beneficial effect also when given with NO-agents(L-NAME+BC 157;L-arginine+BPC 157;L-NAME+L-arginine+BPC 157).Finally,with respect to the increased NO-and MDAvalues-adhesion tissue formation relation,unlike diverse effect of the NO-agents,the BPC 157 application effect regularly combines decrease on the increased NOand MDA-values and the beneficial outcome(less adhesion formation).CONCLUSION BPC 157 therapy can be suited for the realization of the peritoneal defect healing with minimal or no adhesion formation. | Lidija Berkopic Cesar Slaven Gojkovic Ivan Krezic Dominik Malekinusic Helena Zizek Lovorka Batelja Vuletic Andreja Petrovic Katarina Horvat Pavlov Domagoj Drmic Antonio Kokot Josipa Vlainic Sven Seiwerth Predrag Sikiric | 2020 | World Journal of Gastrointestinal Pharmacology and Therapeutics2020，11，5： | 0 |
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