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Introduction: Glucagon-like peptide -1 (GLP-1) is released by intestinal cells to stimulate glucose-dependent insulin release from the pancreas. GLP-1 has been linked to ameliorating obesity and/or diabetic complications as well as controlling reproductive function. Liraglutide is a GLP-1 receptor agonist (GLP-1RA) with 97% homology with GLP-1. The main objective of this study was to investigate the ameliorative role of liraglutide in diabetic-induced reproductive dysfunction in male rats. Methods: Rats were randomly allocated into 3 groups; a control group, a diabetic group, and a liraglutide-treated diabetic group. Results: In the diabetic group, a significant increase in BMI, FBG, HbA1c, HOMA-IR, TC, TAG, LDL, IL6, TNFα, and MDA, as well as decreased serum insulin, HDL, GSH, total testosterone, LH, and FSH, were shown compared to the control group. Furthermore, A significant downregulation in relative hypothalamic gene expression of GLP-1R, PPAR-α, PGC-1α, kiss, kiss1R, leptin, leptin R, GnRH GLP-1R, testicular PGC-1α, PPARα, kiss1, kiss1R, STAR, CYP17A1, HSD17B3, CYP19A, CYP11A1, and Smad7, as well as upregulation in hypothalamic GnIH and testicular TGF- β and Smad2 expression, were noticed compared to the control group. Liraglutide treatment significantly improved such functional and structural reproductive disturbance in diabetic rats. Conclusion: GLP-1RAs ameliorated the deleterious effects of diabetes on reproductive function by targeting GLP-1/leptin/kiss1/GnRH, steroidogenesis, and TGF-ß/Smad pathways. [ABSTRACT FROM AUTHOR]

Background: Liver injury due to ischemia/reperfusion (I/R) is a major challenge during liver surgery. Effects of paeonol pretreatment on partial hepatic I/R injury were assessed in this study. Methods: Male Wistar rats were allocated into sham, vehicle-I/R, and paeonol-I/R groups. Paeonol, 100 mg/kg/day, was administered by gavage. After 10 days, rats of I/R groups were subjected to partial I/R of the liver. Blood samples were collected for assessment of alanine and aspartate aminotransferases as well as gamma glutamyl transferases. Liver samples were taken for detection of tumor necrosis factor-α (TNF-α) and malondialdhyde (MDA) levels as well as superoxide dismutase (SOD) activity. The mRNA expression of toll-like receptor-4 (TLR4), myeloid differentiation factor 88 (MyD88), high mobility group box 1 (HMG-1), and peroxisome proliferator-activated receptor-γ (PPAR-γ) were assessed in the liver. Hematoxylin& eosin stained liver sections were examined. Expressions of nuclear factor kappa B (NF-κB) and autophagy markers (LC3 II, P62) were assessed in immunostained sections. Results: Liver I/R increased serum transferases and tissue MDA, TNF-α, TLR4, HMGB-1, MyD88, NF-κB, LC3 II, P62 levels with hydropic degeneration and cellular infiltration in the liver while decreased SOD activity and PPAR-γ mRNA expression. These alterations were attenuated by paeonol pretreatment. Conclusions: Paeonol pretreatment alleviated liver I/R injury through inhibition of autophagy and TLR4/MyD88/NF-κB pathways. [ABSTRACT FROM AUTHOR]

Background: Non-alcoholic fatty liver disease (NAFLD) is characterized by abnormal fat metabolism in the liver due to nonalcoholic causes. Adropin is a peptide hormone with an essential role in maintaining metabolic homeostasis. Methods: 42 male rats were divided into 2 groups, each group was subdivided into 3 subgroups: group Ia: control 4 weeks; group Ib: high fat diet (HFD) 4 weeks, group Ic: HFD 4 weeks +exercise; group IIa: control 12 weeks, group IIb: HFD 12 weeks; and group IIc: HFD 12 weeks + exercise. Serum Adropin, glucose, HOMA-IR, insulin, lipid profile, ALT, AST, TNFα, IL6, hepatic ROS, MDA, and SOD were measured. Histopathological examination, immunohistochemical study, and Mallory's trichrome staining of the liver were performed. Results: significant increases in insulin resistance, lipid profile parameters, ALT, AST, TNFα, IL6, hepatic ROS, MDA, and a decrease in SOD were found in HFD groups. Histopathological examination revealed steatosis in group Ib and steatohepatitis in group IIb. These changes were associated with a decrease in serum adropin levels. Exercise in groups Ic and IIc improved these changes with a significant increase in adropin level. Conclusion: HFD induced functional and structural deterioration in the liver, leading to NAFLD with a significant decrease in serum adropin level. Exercise induced a significant increase in serum adropin, which may have a role in the remission of hepatic inflammation, steatosis, and steatohepatitis. [ABSTRACT FROM AUTHOR]

Background: Cisplatin is one of the most widely used anticancer drugs. As with most of the chemotherapeutic agents, it doesn't only target cancerous cells but is also distributed to normal cells as well causing many organs toxicity. Being the most important organ in the immune system; the spleen affection by cisplatin treatment must be carefully prevented or reversed. This current study aimed to assess the protective effect of a Notch inhibitor dibenzazepine (DBZ) against cisplatin-induced splenic toxicity as well as explore the proposed mechanism shedding light on the role of the Notch pathway in its effect. Methods: Rats were treated with DBZ (2mg/kg) for 12 days with a single dose of cisplatin (7mg/kg) injected on the 8th day of treatment. Rats were divided into four groups: Control, DBZ, Cisplatin, and DBZ+ Cisplatin group. Results: Cisplatin injection upregulated the oxidative stress markers MDA and iNOS along with reduced antioxidant enzymes glutathione and catalase. The inflammatory markers (TNFα, IL1β, and NKĸB) were also upregulated. Furthermore, the Notch-1 and Hes-1 expressions were also significantly elevated. Cisplatin-induced splenic tissue damage was further assured by light and electron microscopic histopathological examination. DBZ pre-treatment significantly restored the upregulated oxidative stress, and inflammatory as well as Notch signaling pathways toward normal levels. Additionally, the histopathological architecture impairment was improved by Dibenzazepine. Conclusions: The study elucidated that DBZ protects against cisplatin-induced toxicity in rats via antioxidative and antiinflammatory effects. Moreover, downregulating the Notch signaling pathway was proved to play a role in DBZ's protective effect against cisplatin-induced splenic toxicity. [ABSTRACT FROM AUTHOR]

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The main cause of mortality and disability globally is myocardial infarction (MI). Isoproterenol (ISO), a b-adrenoceptor agonist, has been used to induce rat myocardial necrosis. Whereas interleukin-37 (IL-37) has anti-inflammatory and cytoprotective properties. The study aimed to investigate the potential protective effects of IL-37 administration on cardiac architecture, oxidative stress, and inflammatory markers during ISO-induced MI in rats. Three groups of adult male rats were used in this study, the normal control group (n=8), ISO-induced MI group (n=8) that received isoproterenol hydrochloride (ISO) (100 mg/kg/day, SC, for the first 2 consecutive days), and IL-37-treated group (ISO+IL-37) (n=8) that received recombinant human IL-37 (40 mg/kg/day, intraperitoneally, for 2 weeks during and after ISO injections. Heart rate (HR.) and ECG changes were monitored. Some oxidative stress markers such as superoxide dismutase (SOD), nitric oxide (NOx), malondialdehyde (MDA), and glutathione (GSH) tissue levels in the tissue homogenate were assayed. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), caspase-8, P53, and C-reactive protein (CRP) were among the inflammatory markers examined. In addition, serum levels of creatinine kinase (CK-MB) and lactate dehydrogenase (LDH) were analyzed to evaluate the myocardial injury. For histological analysis, tissues were sectioned, fixed in paraffin, and stained with hematoxylin and eosin (H&E), Masson Trichrome and, immunohistochemical against NF-kB, TNF-α, and Caspase-9. IL-37 improved ECG changes, cardiac enzyme markers, and some inflammatory markers of oxidative stress in ISO-induced MI. It also improved the histopathological and immunohistochemical changes in MI. In conclusion: IL-37 might be a promising therapeutic modality in myocardial infarction. [ABSTRACT FROM AUTHOR]