Suprahepatic inferior caval vein occlusion induced portal and caval hypertension, aortic hypotension and esophageal bleeding. therapy with pentadecapeptide BPC 157

Pentadecapeptide BPC 157 is intraduced as therapy in a suprahepatic inferior caval vein (ICV) occlusion 15 min, 24h, 48h after complete ICV ligation. Suprahepatic ICV complications that were counteracted by BPC 157 included esophageal bleeding, severe portal and caval hypertension, and aortal hypotension. Likewise, BPC 157 counteracts the lesions in the whole GI-tract. Medication (BPC 157 (10 μg/kg, 10 ng/kg), or saline (5 ml/kg) (controls)) was applied as an abdominal bath immediately after ICV occlusion. ICV occlusion produced severe esophageal bleeding in all controls, along with microscopy findings. Contrarily, given in ischemic period, BPC 157 counteracts severe esophageal bleeding and maintained grossly intact esophageal mucosa . In rats with ICV occlusion, assessment of portal (PV), caval (ICV) and aortal (AA) pressure showed huge portal hypertension and more caval hypertension, along with mild aortic hypotension (15 min: 68±4 PV, 45±4 ICV, 73±3 AA; 24 h: 56±5 PV, 49±5 ICV, 35±3 AA; 48 h 30±3 PV, 48±5 ICV, 39±3 AA-ligation period). Contrarily, BPC 157 in rats with suprahepatic ICV occlusion markedly counteracted portal and caval hypertension, and arterial hypotension (10 μg/kg bath 15 min: 3±1 PV, 9±1 ICV, 117±5 AA; 24 h: 5±1 PV, 9±1 ICV, 67±5 AA; 48 h: 5±1 PV, 9±1 ICV, 70±6 AA), 10 ng/kg bath produced similar results. BPC 157 therapy successfully counteracts the adverse effects of the suprahepatic ICV occlusion

Splenectomy induced portal and caval hypertension, aortic hypotension, venous thrombosis, peaked p waves, and tachycardia. therapy with pentadecapeptide BPC 157

We introduce BPC 157 therapy for a cluster of complications taking place after splenectomy in rats, including portal vein (PV), inferior vena cava (IVC), superior mesenteric vein (SMV) and lienal vein (LV) thrombosis, severe venous hypertension (PV, IVC), abdominal aorta (AA) hypotension, peaked P waves and tachycardia. Medication (/kg) (BPC 157 (10 μg)(treated group) or saline (5 ml)(control group)) was applied as an abdominal bath immediately after splenectomy. 10min, 3h, and 24h after splenectomy rats were assessed via electrocardiography, USB microcamera, intravascular cannulation, and thrombi extraction. Splenectomized rats exhibited PV and IVC hypertension, aortic hypotension (mmHg) (10min: 65±4 PV, 46±4 IVC, 71±3 AA; 3h: 42±4 PV, 61±4 IVC, 70±3 AA; 24h: 38±4 PV, 47±4 IVC, 68±3 AA) and thrombosis (thrombus weight, mg) (10min: 9.5±0.5 IVC, 6.6±0.9 PV, 4.8±0.9 SMV, 1.3±0.6 LV; 3h: 10.1±0.5 IVC, 5.3±0.8 PV, 19.2±0.9 SMV, 1.0±0.6 LV; 24h: 33.8±2.5 IVC, 27.5±2.9 PV, 8.8±0.9 SMV, 3.8±0.6 LV). BPC 157 normalised blood pressure (10min: 29±4 PV, 20±4 IVC, 87±3 AA; 3h: 20±4 PV, 17±4 IVC, 81±3 AA; 24h: 12±4 PV, 20±4 IVC, 82±3 AA) and reduced thrombosis (10min: 2.9±0.5 IVC, 2.6±0.9 PV, 3.2±0.3 SMV, 0.5±0.2 LV; 3h: 6.3±0.5 IVC, 2.3±0.5 PV, 5.9±0.9 SMV, 0.6±0.2 LV, 24h: 12.2±2.5 IVC, 1.9±0.5 PV, 4.8±0.9 SMV, 2.0±0.6 LV). Control group presented with peaked P waves, tachycardia and PV/SMV congestion, whereas the treated group showed none of the aforementioned phenomena. BPC 157 therapy counteracts hemodynamic disturbances, peaked P waves, and tachycardia as post-splenectomy complications

Stable Gastric Pentadecapeptide BPC 157 in Rats with Episcleral Veins Cauterization, Glaucoma Model, Preserved Retinal and Optic Nerve Integrity

BPC 157 (LD1 not achieved) was implemented as an anti-ulcer peptide in IBD trials and now in a multiple sclerosis trial. BPC 157 maintained corneal transparency, total debridement of corneal epithelium cured with no corneal neovascularization, perforating corneal incisions in rats successfully closed and no new vessels, providing a particular healing and vascular effect. We wanted to explore effect of BPC 157 in rats with glaucoma, induced by episcleral veins cauterization. Randomly assigned operated male Wistar rats, 250g (two dorsal episcleral veins and one temporal episcleral vein isolated from the surrounding tissues; a cautery specifically applied to the selected vein), were further studied. Medication (pentadecapeptide BPC 157 (10μg/kg) (Diagen, Slovenia) intraperitoneally) or an equivolume of 0.9%NaCl (5ml/kg) intraperitoneally (controls)) was applied immediately after surgery, and then once time daily. Histopathological retinal and optic nerve samples were obtained after sacrifice at 24h, 4 and 6-weeks interval. At 24h, 4 and 6 weeks after surgery controls exhibited ganglion cell layer and optic nerve thinning. All BPC 157 rats exhibited only slight or none ganglion cell layer or optic nerve thinning. Pentadecapeptide BPC 157 continuously counteracts the effects of episcleral veins cauterization on morphological changes of ganglion cell layer and optic nerve

Splenectomy induced portal and caval hypertension, aortic hypotension, venous thrombosis, peaked p waves, and tachycardia. therapy with pentadecapeptide BPC 157

We introduce BPC 157 therapy for a cluster of complications taking place after splenectomy in rats, including portal vein (PV), inferior vena cava (IVC), superior mesenteric vein (SMV) and lienal vein (LV) thrombosis, severe venous hypertension (PV, IVC), abdominal aorta (AA) hypotension, peaked P waves and tachycardia. Medication (/kg) (BPC 157 (10 μg)(treated group) or saline (5 ml)(control group)) was applied as an abdominal bath immediately after splenectomy. 10min, 3h, and 24h after splenectomy rats were assessed via electrocardiography, USB microcamera, intravascular cannulation, and thrombi extraction. Splenectomized rats exhibited PV and IVC hypertension, aortic hypotension (mmHg) (10min: 65±4 PV, 46±4 IVC, 71±3 AA; 3h: 42±4 PV, 61±4 IVC, 70±3 AA; 24h: 38±4 PV, 47±4 IVC, 68±3 AA) and thrombosis (thrombus weight, mg) (10min: 9.5±0.5 IVC, 6.6±0.9 PV, 4.8±0.9 SMV, 1.3±0.6 LV; 3h: 10.1±0.5 IVC, 5.3±0.8 PV, 19.2±0.9 SMV, 1.0±0.6 LV; 24h: 33.8±2.5 IVC, 27.5±2.9 PV, 8.8±0.9 SMV, 3.8±0.6 LV). BPC 157 normalised blood pressure (10min: 29±4 PV, 20±4 IVC, 87±3 AA; 3h: 20±4 PV, 17±4 IVC, 81±3 AA; 24h: 12±4 PV, 20±4 IVC, 82±3 AA) and reduced thrombosis (10min: 2.9±0.5 IVC, 2.6±0.9 PV, 3.2±0.3 SMV, 0.5±0.2 LV; 3h: 6.3±0.5 IVC, 2.3±0.5 PV, 5.9±0.9 SMV, 0.6±0.2 LV, 24h: 12.2±2.5 IVC, 1.9±0.5 PV, 4.8±0.9 SMV, 2.0±0.6 LV). Control group presented with peaked P waves, tachycardia and PV/SMV congestion, whereas the treated group showed none of the aforementioned phenomena. BPC 157 therapy counteracts hemodynamic disturbances, peaked P waves, and tachycardia as post-splenectomy complications

Stable Gastric Pentadecapeptide BPC 157 in Rats with Episcleral Veins Cauterization, Glaucoma Model, Preserved Retinal and Optic Nerve Integrity

BPC 157 (LD1 not achieved) was implemented as an anti-ulcer peptide in IBD trials and now in a multiple sclerosis trial. BPC 157 maintained corneal transparency, total debridement of corneal epithelium cured with no corneal neovascularization, perforating corneal incisions in rats successfully closed and no new vessels, providing a particular healing and vascular effect. We wanted to explore effect of BPC 157 in rats with glaucoma, induced by episcleral veins cauterization. Randomly assigned operated male Wistar rats, 250g (two dorsal episcleral veins and one temporal episcleral vein isolated from the surrounding tissues; a cautery specifically applied to the selected vein), were further studied. Medication (pentadecapeptide BPC 157 (10μg/kg) (Diagen, Slovenia) intraperitoneally) or an equivolume of 0.9%NaCl (5ml/kg) intraperitoneally (controls)) was applied immediately after surgery, and then once time daily. Histopathological retinal and optic nerve samples were obtained after sacrifice at 24h, 4 and 6-weeks interval. At 24h, 4 and 6 weeks after surgery controls exhibited ganglion cell layer and optic nerve thinning. All BPC 157 rats exhibited only slight or none ganglion cell layer or optic nerve thinning. Pentadecapeptide BPC 157 continuously counteracts the effects of episcleral veins cauterization on morphological changes of ganglion cell layer and optic nerve

Stable Gastric Pentadecapeptide BPC 157 in Rats with Episcleral Veins Cauterization, Glaucoma Model, Preserved Retinal and Optic Nerve Integrity

BPC 157 (LD1 not achieved) was implemented as an anti-ulcer peptide in IBD trials and now in a multiple sclerosis trial. BPC 157 maintained corneal transparency, total debridement of corneal epithelium cured with no corneal neovascularization, perforating corneal incisions in rats successfully closed and no new vessels, providing a particular healing and vascular effect. We wanted to explore effect of BPC 157 in rats with glaucoma, induced by episcleral veins cauterization. Randomly assigned operated male Wistar rats, 250g (two dorsal episcleral veins and one temporal episcleral vein isolated from the surrounding tissues; a cautery specifically applied to the selected vein), were further studied. Medication (pentadecapeptide BPC 157 (10μg/kg) (Diagen, Slovenia) intraperitoneally) or an equivolume of 0.9%NaCl (5ml/kg) intraperitoneally (controls)) was applied immediately after surgery, and then once time daily. Histopathological retinal and optic nerve samples were obtained after sacrifice at 24h, 4 and 6-weeks interval. At 24h, 4 and 6 weeks after surgery controls exhibited ganglion cell layer and optic nerve thinning. All BPC 157 rats exhibited only slight or none ganglion cell layer or optic nerve thinning. Pentadecapeptide BPC 157 continuously counteracts the effects of episcleral veins cauterization on morphological changes of ganglion cell layer and optic nerve

Pentadecapeptide BPC 157 Counteracts the Adverse Effects of Lithium Overdose in Rats

INTRODUCTION We sought to determine whether stable gastric pentadecapeptide BPC 157 mitigates lithium intoxication in rats. METHODS: Lithium was applied at 500 mg/kg/day, intraperitoneally, once daily throughout 3 subsequent days. Medication used (in mg/kg) for the treatment group includes BPC 157 (0.01; 0.00001), L-NAME (5.0), L-arginine (100.0), applied alone and/or together, while control group rats received an equivolume of saline solution (5 mL/kg). At 20 minutes after drug application, we assessed muscular weakness (score 1-5) during the following 8 minutes. Then, for the next 5 minutes, we recorded an ECG. At 3 hours after that, the brain, the heart, the quadriceps muscle and the diaphragm muscle were used for histopathological analysis. RESULTS Consistently, lithium produced severe intoxication syndrome (muscular weakness and prostration, reduced quadriceps muscle fibers and diaphragm, myocardial infarction, and edema of various brain areas, most prominently in the cerebral cortex). The effects worsening with subsequent applications. L-NAME and L-arginine, given separately, both induced severe aggravation. This aggravation disappeared when L-NAME and L-arginine were given together. Contrarily, when given alone or together with NO-agents, BPC 157 reduced muscular weakness and prostration and muscle damage and mitigated lithium induced myocardial damage. BPC 157 reduced nerve damage and brain edema. CONCLUSION BPC 157 could be used as therapy for lithium intoxication

Pentadecapeptide BPC 157 counteracts portal hypertension, caval hypertension and aortal hypotension with suprahepatic occlusion of inferior caval vein in rats

Portal hypertension, aortal hypotension, caval hypertensio

Pentadecapeptide BPC 157 Counteracts the Adverse Effects of Lithium Overdose in Rats

INTRODUCTION We sought to determine whether stable gastric pentadecapeptide BPC 157 mitigates lithium intoxication in rats. METHODS: Lithium was applied at 500 mg/kg/day, intraperitoneally, once daily throughout 3 subsequent days. Medication used (in mg/kg) for the treatment group includes BPC 157 (0.01; 0.00001), L-NAME (5.0), L-arginine (100.0), applied alone and/or together, while control group rats received an equivolume of saline solution (5 mL/kg). At 20 minutes after drug application, we assessed muscular weakness (score 1-5) during the following 8 minutes. Then, for the next 5 minutes, we recorded an ECG. At 3 hours after that, the brain, the heart, the quadriceps muscle and the diaphragm muscle were used for histopathological analysis. RESULTS Consistently, lithium produced severe intoxication syndrome (muscular weakness and prostration, reduced quadriceps muscle fibers and diaphragm, myocardial infarction, and edema of various brain areas, most prominently in the cerebral cortex). The effects worsening with subsequent applications. L-NAME and L-arginine, given separately, both induced severe aggravation. This aggravation disappeared when L-NAME and L-arginine were given together. Contrarily, when given alone or together with NO-agents, BPC 157 reduced muscular weakness and prostration and muscle damage and mitigated lithium induced myocardial damage. BPC 157 reduced nerve damage and brain edema. CONCLUSION BPC 157 could be used as therapy for lithium intoxication

Stable Gastric Pentadecapeptide BPC 157 in Rats with Episcleral Veins Cauterization, Glaucoma Model, Preserved Retinal and Optic Nerve Integrity

BPC 157 (LD1 not achieved) was implemented as an anti-ulcer peptide in IBD trials and now in a multiple sclerosis trial. BPC 157 maintained corneal transparency, total debridement of corneal epithelium cured with no corneal neovascularization, perforating corneal incisions in rats successfully closed and no new vessels, providing a particular healing and vascular effect. We wanted to explore effect of BPC 157 in rats with glaucoma, induced by episcleral veins cauterization. Randomly assigned operated male Wistar rats, 250g (two dorsal episcleral veins and one temporal episcleral vein isolated from the surrounding tissues; a cautery specifically applied to the selected vein), were further studied. Medication (pentadecapeptide BPC 157 (10μg/kg) (Diagen, Slovenia) intraperitoneally) or an equivolume of 0.9%NaCl (5ml/kg) intraperitoneally (controls)) was applied immediately after surgery, and then once time daily. Histopathological retinal and optic nerve samples were obtained after sacrifice at 24h, 4 and 6-weeks interval. At 24h, 4 and 6 weeks after surgery controls exhibited ganglion cell layer and optic nerve thinning. All BPC 157 rats exhibited only slight or none ganglion cell layer or optic nerve thinning. Pentadecapeptide BPC 157 continuously counteracts the effects of episcleral veins cauterization on morphological changes of ganglion cell layer and optic nerve