scholarly journals Pistacia Terebinthus Coffee Protects against Thioacetamide-Induced Liver Injury in Rats

2015 ◽  
Vol 58 (2) ◽  
pp. 56-61 ◽  
Author(s):  
Ibrahim Halil Bahçecıoğlu ◽  
Murat Ispiroglu ◽  
Mehmet Tuzcu ◽  
Cemal Orhan ◽  
Mustafa Ulas ◽  
...  
Keyword(s):  
Liver Injury ◽  
Transforming Growth Factor Beta ◽  
Unsaturated Fatty Acids ◽  
Transforming Growth Factor ◽  
Tap Water ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Pistacia Terebinthus

Aim/background: Pistacia terebinthus is used as a coffee substitute in the East and Southern Anatolia regions of Turkey. It contains unsaturated fatty acids, tocopherols, polyphenols and carotenoids. P. terebinthus has anti-inflammatory and potential antioxidant activity. In this study we evaluated the protective effects of P. terebinthus coffee (PTC) on thioacetamide (TAA)-induced liver injury in rats. Materials and methods: Twenty-eight male Sprague-Dawley rats were equally randomized into four groups. Chronic liver injury was induced with TAA (100 mg/kg i.p. three times weekly). The first group of rats served as control and received only tap water (G1), and the remaining groups of rats received PTC, p.o (G2); TAA (G3); TAA plus PTC, p.o (G4), respectively. Results: After 8 weeks, PTC intake significantly reduced fibrosis/inflammation scores (p < 0.05) in the livers of TAA-treated group. Compared to control group, PTC intake reduced transforming growth factor beta (TGF-β) concentrations in the liver (p < 0.05). Compared to the TAA group, TGF-β, nuclear factor kappa B (NF)-κB (p < 0.05), tumor necrosis factor alpha (TNF-α) concentrations in the liver tissue were reduced by PTC intake. Discussion and conclusion: PTC intake provided beneficial effects against TAA-induced liver injury in rats. PTC probably suppresses the proinflammatory cytokines through NF-κB signaling pathway.

Protective effect of an L-type calcium channel blocker, amlodipine, on paracetamol-induced hepatotoxicity in rats

2018 ◽  
Vol 37 (11) ◽  
pp. 1169-1179 ◽  
Author(s):  
H Kaya ◽  
B Polat ◽  
A Albayrak ◽  
T Mercantepe ◽  
B Buyuk
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Transforming Growth Factor Beta ◽  
Channel Blocker ◽  
Transforming Growth Factor ◽  
Histopathological Examination ◽  
Control Group ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Paracetamol (P), one of the most popular and commonly used analgesic and antipyretic agents, causes hepatotoxicity in overdoses. Amlodipine (AML), an L-type calcium channel blocker, has been shown to have anti-inflammatory activity by reversing the effect of calcium in the inflammation pathogenesis. In this study, the hepatoprotective activity of AML on P-induced hepatotoxicity was evaluated. Thirty male albino Wistar rats were divided into five groups: (1) control, (2) 2 g/kg of P, (3) 2 g/kg of P + 5 mg/kg of AML, (4) 2 g/kg of P + 10 mg/kg of AML, and (5) 10 mg/kg of AML. Some liver enzymes, oxidative parameters, cytokine mRNA expressions, histopathology, and immunohistochemical studies were performed in liver and blood samples. The serum levels of alanine aminotransferase and aspartate aminotransferase and the mRNA expression of tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta in the liver tissues were significantly increased in the group treated with P. The superoxide dismutase and glutathione parameters decreased and malondialdehyde levels increased in the livers of the rats treated with P. All these parameters were increased with both doses of the AML similar to the control group. A histopathological examination of the liver showed that AML administration ameliorated the P-induced inflammatory liver damage. In immunohistochemical staining, the expression of TNF-α in the cytoplasm of the hepatocytes was increased in the P group but not in other treatment groups when compared to the control. In conclusion, AML treatment showed significant protective effects against P-induced hepatotoxicity by increasing the activity of antioxidants and reducing inflammatory cytokines.

scholarly journals Role of endocannabinoid CB1 receptors in Streptozotocin-induced uninephrectomised Wistar rats in diabetic nephropathy

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Jayarami Reddy Medapati ◽  
Deepthi Rapaka ◽  
Veera Raghavulu Bitra ◽  
Santhosh Kumar Ranajit ◽  
Girija Sankar Guntuku ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Morphological Changes ◽  
Serum Levels ◽  
Cb1 Receptors ◽  
Protective Effects ◽  
Renal Hypertrophy ◽  
Necrosis Factor Alpha

Abstract Background The endocannabinoid CB1 receptor is known to have protective effects in kidney disease. The aim of the present study is to evaluate the potential agonistic and antagonistic actions and to determine the renoprotective potential of CB1 receptors in diabetic nephropathy. The present work investigates the possible role of CB1 receptors in the pathogenesis of diabetes-induced nephropathy. Streptozotocin (STZ) (55 mg/kg, i.p., once) is administered to uninephrectomised rats for induction of experimental diabetes mellitus. The CB1 agonist (oleamide) and CB1 antagonist (AM6545) treatment were initiated in diabetic rats after 1 week of STZ administration and were given for 24 weeks. Results The progress in diabetic nephropathy is estimated biochemically by measuring serum creatinine (1.28±0.03) (p < 0.005), blood urea nitrogen (67.6± 2.10) (p < 0.001), urinary microprotein (74.62± 3.47) (p < 0.005) and urinary albuminuria (28.31±1.17) (p < 0.0001). Renal inflammation was assessed by estimating serum levels of tumor necrosis factor alpha (75.69±1.51) (p < 0.001) and transforming growth factor beta (8.73±0.31) (p < 0.001). Renal morphological changes were assessed by estimating renal hypertrophy (7.38± 0.26) (p < 0.005) and renal collagen content (10.42± 0.48) (p < 0.001). Conclusions From the above findings, it can be said that diabetes-induced nephropathy may be associated with overexpression of CB1 receptors and blockade of CB1 receptors might be beneficial in ameliorating the diabetes-induced nephropathy. Graphical abstract

Maternal Sodium Valproate Exposure Alters NeuroendocrineCytokines and Oxido-inflammatory Axes in Neonatal Albino Rats

2020 ◽  
Vol 20 ◽  
Author(s):  
Naama A-G ◽  
El-bakry AM ◽  
Rasha EH ◽  
Ahmed RG
Keyword(s):  
Growth Factor ◽  
Sodium Valproate ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Control Group ◽  
Albino Rats ◽  
Serum Growth Hormone ◽  
Pregnant Rats ◽  
Necrosis Factor Alpha ◽  
Insulin Growth Factor

Objective: he aim of the study was to determine the influence of maternal sodium valproate (SVP) on neonatal neuroendocrine (hypothalamic-pituitary-adrenal; HPA)-cytokines and oxido-inflammatory axes. Methods: Pregnant rats (Rattus norvegicus) were orally administered (by gavage) SVP (50 mg/kg) from gestation day (GD) 8 to lactation day (LD) 21. Results: The elevation in serum corticotropin-releasing hormone (CRH), corticosterone, and adrenocorticotropic hormone (ACTH) levels was highly significant at postnatal days (PNDs) 14 and 21 in both dams and neonates of the maternal SVPtreated group relative to those in the control group. However, hypercortisolism (cortisolemia) was highly significant in neonates at both PNDs 14 and 21 while in dams, it was not significantly increased at LD 14 but was at LD 21. This disruption caused adverse effects on maternal food consumption and maternal/neonatal body weight. The maternal SVP treatment resulted in higher levels of neonatal serum adrenaline, noradrenaline, neuropeptide Y (NPY), tumor necrosis factor-alpha (TNF-α), leptin, interleukins (IL-1β, IL-17, IL-4, IL-6 & IL-2), transforming growth factor-beta (TGF-β), and prostaglandin E2 (PGE2), and lower levels of neonatal serum growth hormone (GH), insulin growth factor-1 (IGF-1) and adiponectin at both PNDs. This administration also induced the oxidative stress in neonatal cerebrum and cerebellum at both tested PNDs via the production of free radicals (malondialdehyde; MDA & nitric oxide; NO) and reduction of antioxidant parameters (glutathione; GSH, superoxide dismutase; SOD & catalase; CAT). Conclusion: Maternal SVP treatment stimulated neonatal stress-brain (HPA) axis, resulted in an oxido-inflammatory state, and disrupted the neuroendocrine-cytokines axis, and generally neonatal health.

Protective effects of olmesartan and l-carnitine on doxorubicin-induced cardiotoxicity in rats

2020 ◽  
Vol 98 (4) ◽  
pp. 183-193 ◽  
Author(s):  
Malek M. Aziz ◽  
Mai A. Abd El Fattah ◽  
Kawkab A. Ahmed ◽  
Helmy M. Sayed
Keyword(s):  
Transforming Growth Factor Beta ◽  
Troponin I ◽  
Transforming Growth Factor ◽  
Antineoplastic Agent ◽  
The Other ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Group I ◽  
Creatine Kinase Mb

Doxorubicin (DOX), an anthracycline antibiotic, is an important antineoplastic agent due to its high antitumor efficacy in hematological as well as in solid malignancies. The clinical use of DOX is limited due to its cardiotoxic effects. The present study aimed to investigate the possible protective effect of olmesartan (Olm), l-carnitine (L-CA), and their combination in cardiotoxicity induced by DOX in rats. Male albino rats were randomly divided into seven experimental groups (n = 8): group I: normal control, group II: L-CA, group III: Olm, group IV: DOX. The other three groups were treated with Olm (10 mg/kg), L-CA (300 mg/kg), and their combination for 2 weeks after induction of cardiotoxicity by a single dose of DOX (20 mg/kg). In the results, DOX showed a significant elevation in serum troponin I, creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH) together with increased inflammation manifested by the rise of tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecules-1 (ICAM-1), interleukin IL-1β (IL-1β), myeloperoxidase (MPO), nuclear factor-kappa B (NF-κB), and transforming growth factor beta (TGF-β) in cardiac tissues as well as DOX-induced oxidative stress by increasing in malondialdehyde (MDA) and decreasing in superoxide dismutase (SOD) and glutathione (GSH) in heart tissues. In addition, caspase-3 activity was boosted as indication of increased apoptosis. On the other hand, administration of L-CA and Olm attenuated the DOX-evoked disturbances in the abovementioned parameters. In addition, DOX exhibited echocardiographic changes and severe histopathological changes, which were significantly reversed by L-CA and Olm treatment. In conclusion, the present study data confirm the protective role of L-CA and Olm in DOX-induced cardiotoxicity, which may be related to its antioxidant, antiinflammatory, and antiapoptotic agents.

PAI-1 gene 4G/5G polymorphism, cytokine levels and their relations with metabolic parameters in obese children

2008 ◽  
Vol 99 (02) ◽  
pp. 352-356 ◽  
Author(s):  
Muammer Yuce ◽  
Ayse Yazici ◽  
Hasibe Verdi ◽  
F. Belgin Ataç ◽  
Sibel Kinik ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Model Assessment ◽  
Obese Children ◽  
Plasminogen Activator Inhibitor 1 ◽  
Necrosis Factor Alpha ◽  
Pai 1

SummaryObesity is associated with the changes of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNFα) and transforming growth factor beta (TGFβ) levels. However, the precise effect of the 4G allele on obesity is still contradictory. Here, we aimed to elucidate the role of the 4G/5G polymorphism of the PAI-1 gene on the PAI-1 level and determine the associations between cytokines, glucose and lipid metabolism parameters in obese children. Thirty-nine obese children (mean age 11.4 ± 3.3 years) and 38 age-matched healthy control group (mean age 10.3 ± 3.5 years) were included in the study. In all cases, serum levels of glucose, lipid and insulin were measured, homeostasis model assessment of insulin resistance (HOMAIR) was calculated, and 4G/5G polymorphism of PAI-1 gene, plasma PAI-1 level and serum TNFα and TGFβ levels were studied. The mean relative body mass index (BMI) and HOMA-IR score, VLDL,TG, insulin, PAI-1,TNFα levels were higher, and HDL and TGFβ levels were lower in the obese group. The frequency of the 4G/4G genotype was considerably higher in obese children than in controls. Also, a positive correlation was found between PAI-1 and TNFα levels, and relative BMI, HOMA-IR score, insulin,TG, HDL levels. TGFβ was inversely correlated only with relative BMI. There was no correlation among three cytokines. In conclusion, childhood obesity contributes to higher PAI-1 andTNFα and lowerTGFβ levels. Especially PAI-1 andTNFα accompany insulin resistance and dyslipidemia.

scholarly journals Renoprotective Effect of Platelet-Rich Plasma on Cisplatin-Induced Nephrotoxicity in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Neveen Salem ◽  
Nawal Helmi ◽  
Naglaa Assaf
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Platelet Rich Plasma ◽  
Male Rats ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Protective Effects ◽  
Intercellular Adhesion Molecule 1 ◽  
Histopathological Investigation

Platelet-rich plasma (PRP) has grown as an attractive biologic instrument in regenerative medicine for its powerful healing properties. It is considered as a source of growth factors that may induce tissue repairing and improve fibrosis. This product has proven its efficacy in multiple studies, but its effect on cisplatin-induced nephrotoxicity has not yet been elucidated. The present investigation was performed to estimate the protective impact of platelet-rich plasma against cisplatin- (CP-) evoked nephrotoxicity in male rats. Nephrotoxicity was induced in male Wistar rats by right uninephrectomy followed by CP administration. Uninephrectomized rats were assigned into four groups: (1) control group, (2) PRP group, (3) CP group, and (4) CP + PRP group. PRP was administered by subcapsular renal injection. Renal function, inflammatory cytokines, and growth factor level as well as histopathological investigation were carried out. Treatment with PRP attenuated the severity of CP-induced nephrotoxicity as evidenced by suppressed creatinine, blood urea nitrogen (BUN), and N-acetyl glucosaminidase (NAG) levels. Moreover, PRP depressed intercellular adhesion molecule-1 (ICAM-1), kidney injury molecule-1 (KIM-1), caspase-3, and transforming growth factor-beta 1 (TGF-β1) levels, while enhanced the epidermal growth factor (EGF) level. These biochemical results were reinforced by the histopathological investigation, which revealed restoration of normal renal tissue architectures. These findings highlight evidence for the possible protective effects of PRP in a rat model of CP-induced nephrotoxicity, suggesting a new avenue for using PRP to improve the therapeutic index of cisplatin.

Genetic Modifiers of Cerebrovascular Large Vessel Stenosis in Sickle Cell Anemia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1658-1658 ◽  
Author(s):  
M. Catherine Driscoll ◽  
Joseph Devaney ◽  
Heather Gordish ◽  
Caterina Minniti ◽  
Eric P. Hoffman
Keyword(s):  
Candidate Genes ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Large Vessel ◽  
Control Group ◽  
Plasminogen Activator Inhibitor 1 ◽  
Necrosis Factor Alpha ◽  
Vessel Stenosis

Abstract Cerebrovascular disease is a common complication in sickle cell anemia (SCA) with overt stroke occuring in 10% of patients and silent stroke in 24% of patients by age 20 years. Etiologies of overt stroke in SCA are heterogenous and include stenosis of large arteries, hemorrhage, hypertensive and hypoxic encephalopathy. Candidate genes identified as possible modifiers of overt stroke in SCA include adenylate cyclase 9 (ADCY9, rs731471 intron C/T), endothelin-converting enzyme (ECE-1, rs212527, intron A/G), Klotho (KL, rs480780, intron C/A), plasminogen activator inhibitor-1 (PAI-1, rs1799768, − 675 4/5,), transforming growth factor beta receptor 3 (TGFBR3, rs284157, intron G/A), tumor necrosis factor alpha (TNF, rs1800629,-308 G/A), and interlukin 4 receptor (IL4R, rs1805015, 503S/P). We examined the association of these candidate genes in a cohort of patients with SCA and stenosis of large cerebral vessels who are followed at a single institution. Patients with stenosis (n = 42, male = 22) were identified as having overt stroke (n = 29) or positive transcranial Doppler (TCD) (n = 13). The mean age at time of stroke or (+) TCD was 7.8 years. All had large vessel stenosis on magnetic resonance angiogram imaging (MRA). A control group of patients with SCA and normal TCD were identified (n = 71, males = 46, mean age = 14.8 years).This control group has passed through the peak years of stroke risk, ages 2–10 years. Single nucleotide polymorphisms (SNPs) were genotypic using novel Taqman assays. Genotypic associations were determined using logistic regression analysis with odds ratios (OR), 95% confidence intervals, and p-values reported. Among the candidate genes only ADYC9 (OR = 2.75, CI 1.2–6.3, p = 0.017) and TGFBR3 (OR = 2.33, CI 1.0–5.3, p = 0.043) had significant association with stenosis of large vessels in SCA. ADYC9 is a membrane-associated enzyme that catalyzes cAMP formation, which is critical for neuronal signaling and survival. TGFBR3 has a role in cardiac endothelial cell transformation to mesenchyme. Genotypic studies of a complex trait such as stroke in SCA will eventually lead to early diagnosis and new or early interventions. However, such genetic studies require clear definitions of phenotypic subtypes based on neuroimaging studies, including MRA.

scholarly journals Adalimumab Ameliorates Abdominal Aorta Cross Clamping Which Induced Liver Injury in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Erkan Cure ◽  
Medine Cumhur Cure ◽  
Levent Tumkaya ◽  
Yildiray Kalkan ◽  
Ibrahim Aydin ◽  
...  
Keyword(s):  
Liver Injury ◽  
Abdominal Aorta ◽  
Liver Tissue ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels

The aim of this study was to investigate the possible protective effects of adalimumab (ADA) on cell damage in rat liver tissue during ischemia/reperfusion (I/R) injury of infrarenal abdominal aorta. Thirty male Wistar-albino rats were divided into three groups: control, I/R, and I/R+ADA, each group containing 10 animals. Laparotomy without I/R injury was performed in the control group animals. Laparotomy in the I/R group was followed by two hours of infrarenal abdominal aortic cross ligation and then two hours of reperfusion. ADA (50 mg/kg) was administered intraperitoneally as a single dose, to the I/R+ADA group, five days before I/R. The tumor necrosis factor-alpha (TNF-α) (pg/mg protein) and nitric oxide (NO) (µmol/g protein) levels in the I/R group (430.8 ± 70.1, 8.0 ± 1.1, resp.) were significantly higher than those in the I/R+ADA group (338.0 ± 71.6,P=0.006; 6.3 ± 1.2,P=0.008) and the control group (345.5 ± 53.3,P=0.008; 6.5 ± 1.5,P=0.010, resp.). I/R causes severe histopathological injury to the liver tissue, but ADA leads to much less histopathological changes. ADA treatment significantly decreased the severity of liver I/R injury. ADA pretreatment may have protective effects on experimental liver injury.

scholarly journals Wound Healing Effects of Prunus yedoensis Matsumura Bark in Scalded Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Jin-Ho Lee ◽  
Kyungjin Lee ◽  
Mi-Hwa Lee ◽  
Bumjung Kim ◽  
Khanita Suman Chinannai ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Tissue Regeneration ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Control Group ◽  
Sprague Dawley ◽  
Tissue Proliferation ◽  
Inflammatory Phase ◽  
Prunus Yedoensis

Pruni Cortex has been used to treat asthma, measles, cough, urticaria, pruritus, and dermatitis in traditional Korean medicine. The objective of this study was to investigate the effects of Prunus yedoensis Matsumura bark methanol extract (PYE) on scald-induced dorsal skin wounds in rats. Scalds were produced in Sprague-Dawley rats with 100°C water and treated with 5% and 20% PYE (using Vaseline as a base), silver sulfadiazine (SSD), and Vaseline once a day for 21 days, beginning 24 hours after scald by treatment group allocation. The PYE-treated groups showed accelerated healing from 12 days after scald, demonstrated by rapid eschar exfoliation compared to the control and SSD groups. PYE-treated groups showed higher wound contraction rates and better tissue regeneration in comparison with the control group. Serum analysis showed that transforming growth factor beta 1 and vascular endothelial growth factor levels remained high or gradually increased up to day 14 in both PYE groups and then showed a sharp decline by day 21, implying successful completion of the inflammatory phase and initiation of tissue regeneration. These findings suggested that PYE is effective in promoting scald wound healing in the inflammation and tissue proliferation stages.

scholarly journals Metabolomics Profiling to Investigate the Pharmacologic Mechanisms of Berberine for the Treatment of High-Fat Diet-Induced Nonalcoholic Steatohepatitis

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Jian Li ◽  
Zezhou Liu ◽  
Mingxing Guo ◽  
Kejia Xu ◽  
Miao Jiang ◽  
...  
Keyword(s):  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Unsaturated Fatty Acids ◽  
Treated Group ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
High Fat ◽  
Group I ◽  
Tof Ms

Objective. Berberine has been used to treat nonalcoholic steatohepatitis (NASH), which has been addressed in many studies. In this study, we investigated the molecular pharmacology mechanisms of berberine using metabolomic techniques.Methods. Sprague-Dawley rats were randomly divided into three groups (10 rats in each group): (i) normal control group; (ii) high-fat diet- (HFD-) induced NASH model group; and (iii) HFD berberine-treated group (i.d. 200 mg/kg). The handling procedure lasted eight weeks. Then, UPLC-Q-TOF/MS techniques coupled with histopathology and biochemical analyses were adopted to explore the mechanisms of berberine on the protective effects against NASH.Key Findings. (i) According to conventional test results, berberine treatment plays a fighting role in HFD-induced NASH due to its beneficial effects against insulin resistance, inflammation, and lipid metabolism. (ii) Based on UPLC-Q-TOF/MS techniques, metabolic profiles that involved sphingomyelin (SM), phosphatidylcholine (PC), lysophosphatidylcholine (LysoPC), 13-hydroperoxy-9, 11-octadecadienoic acid (13-HpODE), eicosatrienoic acid, docosatrienoic acid, and eicosenoic acid could provide potential metabolic biomarkers to address the pharmacological mechanisms of berberine.Conclusions. The parts of molecular pharmacological mechanisms of berberine for NASH treatment are related to the regulation of metabolic disruption involving phospholipid and unsaturated fatty acids in rats with NASH.

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