Takotsubo syndrome (TTS) is an acute heart failure syndrome characterised by catecholamine-induced oxidative tissue damage. Punica granatum, a fruit-bearing tree, is known to have high polyphenolic content and has been proven to be a potent antioxidant. This study aimed to investigate the effects of pomegranate peel extract (PoPEx) pre-treatment on isoprenaline-induced takotsubo-like myocardial injury in rats. Male Wistar rats were randomised into four groups. Animals in the PoPEx(P) and PoPEx + isoprenaline group (P + I) were pre-treated for 7 days with 100 mg/kg/day of PoPEx. On the sixth and the seventh day, TTS-like syndrome was induced in rats from the isoprenaline(I) and P + I groups by administering 85 mg/kg/day of isoprenaline. PoPEx pre-treatment led to the elevation of superoxide dismutase and catalase (p < 0.05), reduced glutathione (p < 0.001) levels, decreased the thiobarbituric acid reactive substances (p < 0.001), H₂O₂, O₂⁻ (p < 0.05), and NO₂⁻ (p < 0.001), in the P + I group, when compared to the I group. In addition, a significant reduction in the levels of cardiac damage markers, as well as a reduction in the extent of cardiac damage, was found. In conclusion, PoPEx pre-treatment significantly attenuated the isoprenaline-induced myocardial damage, primarily via the preservation of endogenous antioxidant capacity in the rat model of takotsubo-like cardiomyopathy.

Background: Myocardial injury (MI) is characterized by an increased level of at least one cardiac troponin. Experimental MI can be induced by isoprenaline, a β-adrenergic agonist, and it can lead to heart failure (HF). Liraglutide is glucagon-like 1 peptide receptor agonist used in diabetes management, but it has anti-inflammatory and antioxidative effects, which can be beneficial in treatment of HF. The aim of this study was to investigate the effects of liraglutide on isoprenaline-induced MI and prevention of HF. Methods: Male Wistar albino rats were divided into four groups: Con—received saline the first 2 days + saline the next 7 days; Iso—isoprenaline the first 2 days + saline the next 7 days; Lir—saline the first 2 days + liraglutide the next 7 days; Iso + Lir—isoprenaline the first 2 days + liraglutide the next 7 days. On day 10, blood samples were taken for biochemical analysis and oxidative stress marker evaluation, and hearts were isolated for pathohistological analysis. Cardiac function was assessed by electrocardiography (ECG) and echocardiography (ECHO). Results: Liraglutide treatment significantly attenuated oxidative stress, repaired ECG and ECHO parameters, and mitigated myocardial morphological changes induced by isoprenaline. Conclusions: Liraglutide restores cardiac function in isoprenaline-induced HF.

Diabetes mellitus (DM) and inflammatory bowel disease (IBD) are prevalent chronic conditions characterized by immune dysregulation and metabolic disturbances. The global incidence of both diseases is increasing, with mounting evidence highlighting the critical role of intestinal barrier dysfunction and inflammation in their pathogenesis. Although genome-wide association studies (GWAS) have implicated the orosomucoid-like protein 3 ( ORMDL3 ), also known as ORMDL sphingolipid biosynthesis regulator 3, in susceptibility to both IBD and DM, its precise role in diabetes-associated intestinal alterations remains poorly defined. In this study, we examined intestinal changes in a Sprague Dawley rat model of experimentally induced diabetes, focusing on ORMDL3 expression and its relationship with endoplasmic reticulum (ER) stress and autophagy. Diabetic rats exhibited pronounced histopathological alterations, including villous atrophy, goblet cell depletion, inflammatory cell infiltration, and lipofuscin accumulation, indicative of compromised intestinal barrier integrity and chronic low-grade inflammation. ORMDL3 expression was significantly elevated at both the transcript and protein levels. A strong positive correlation between ORMDL3 and ATF6 suggests the activation of ER stress pathways within the diabetic intestine. Additionally, increased expression of autophagy-related genes, including NOD2 , ULK1 , and ATG4 , was particularly evident in female diabetic rats, indicating a sex-specific modulation of autophagic responses to hyperglycemic stress. The observed molecular and histological changes reflect key mechanisms implicated in IBD, potentially indicating shared pathways driving both diabetic and inflammatory intestinal disorders. Collectively, our findings underscore a complex interplay between hyperglycemia-induced ER stress and autophagy in the diabetic intestine, positioning ORMDL3 as an orchestrator in the underlying pathogenesis and a potential therapeutic target for IBDs.

Diabetes mellitus and inflammatory bowel disease are chronic inflammatory disorders characterized by immune dysregulation and rising global prevalence. Epidemiological studies increasingly suggest a bidirectional association between the two conditions, linked through shared mechanisms of intestinal barrier dysfunction, microbial dysbiosis, and sustained innate immune activation. Activated macrophages play a central role in driving mucosal inflammation through polarization toward a pro-inflammatory M1 phenotype, accompanied by increased production of inflammatory cytokines. These mediators disrupt tight junctions, induce epithelial apoptosis, and perpetuate cycles of immune activation and tissue injury. This macrophage–cytokine axis not only amplifies local inflammation but also sustains chronic barrier dysfunction, creating a pathogenic overlap between diabetes mellitus-associated intestinal injury and intestinal bowel disease. In this study, we used a low dose streptozotocin and high-fat diet-induced diabetic Sprague–Dawley rat model in both sexes to investigate the effects of chronic hyperglycemia on intestinal inflammation, with particular emphasis on macrophage activation and pro-inflammatory cytokine responses. We found inflammation in both small and large intestines with mucosal injury and barrier disruption, and immune activation involving macrophages and enhanced expression of CD68, iNOS, TNF-α, and IL-6. Female rats were more susceptible to gut-related inflammatory changes due to diabetes. These findings suggest a complex interplay between epithelial stress, immune signaling, and microbial factors supporting the role of intestinal inflammation in the immune–metabolic interaction in diabetes-associated intestinal changes, which may contribute to the pathogenesis of inflammatory bowel disease.

Acute mesenteric ischemia (AMI) is a life-threatening condition characterised by oxidative stress, inflammation, apoptosis, and necrosis of intestinal epithelial cells. Different drugs with vasoactive, antioxidant, and anti-inflammatory properties have been used to treat AMI. Levosimendan is a drug with proven anti-ischemic effects used in the management of acute congestive heart failure. This study evaluated the protective effects of levosimendan pretreatment on intestinal, as well as lung, heart, and kidney tissue in a rat model of mesenteric artery ischemia/reperfusion (I/R) injury. Male Wistar rats (N = 24) were divided into four groups: control, I/R, levosimendan (LS) 1 mg/kg i.p, and LS + I/R (1 mg/kg i.p. 30 min before injury). I/R by itself caused elevation of oxidative markers (thyobarbituric acid reactive species (TBARS), hydrogen peroxide (H₂O₂), super oxide anjon radical (O₂⁻), and nitrogen dioxide (NO₂⁻)), induced inflammation (macrophage infiltration and Interleukin-6 (IL-6) production), and apoptosis (nuclear factor kappa light-chain enhancer of activated B cells (NF-κB), cleaved caspase-3 (CC3), and terminal deoxy-nucleotidyl transferase (TdT)-mediated dUTP nick end labelling (TUNEL)). Levosimendan pretreatment significantly reduced oxidative stress markers and enhanced antioxidant defences (catalase (CAT), reduced glutathione (GSH), and superoxide dismutase (SOD)). Histological analysis revealed reduced mucosal damage and preserved goblet cells in intestinal tissue. Similar protective effects of levosimendan were observed in other organs such as lung, heart, and kidney. Immunohistochemistry showed reduced epithelial apoptosis and upregulation of antioxidant and anti-inflammatory proteins. These findings highlight levosimendan’s ability to protect mesenteric I/R tissue injury and multi-organ damage by suppressing oxidative stress, inflammation, and apoptosis, emphasising its therapeutic potential in clinical settings.

Acute mesenteric ischaemia (AMI) is a serious disease with mortality between 50 and 80 %. Oxidative stress plays a major role in the pathophysiology of AMI. AMI should be considered for any acute abdominal pain that requires analgesia with morphine and for which no other obvious aetiology is found. CT is the main diagnostic procedure to confirm the diagnosis of AMI. There is no specific diagnostic biomarker for AMI that can be used in routine practice. AMI is an urgent diagnostic and therapeutic situation. Treatment of AMI includes a protocol combining digestive rest, curative anticoagulant, antiplatelet, antibiotic therapy, arterial revascularisation to salvage viable bowel and resection of necrotic digestive segments. The strategy of revascularisation depends on the mechanism of arterial occlusion, the morphological appearance of the lesions and the indications for exploratory laparotomy. Endovascular and open surgical techniques can be combined and complemented. Open surgical revascularisation is indicated in case of failure or impossibility of endovascular revascularisation and in case of need for laparotomy. Early diagnosis and timely surgical intervention are the cornerstones of modern treatment to reduce the high mortality of AMI. The emergence of endovascular approaches and modern imaging techniques is developing and providing new treatment options. A multidisciplinary approach based on early diagnosis and treatment is necessary.