scholarly journals Antioxidative role of selected herbs against ethanol induced liver injury in rats

2011 ◽  
Vol 3 (2) ◽  
pp. 242-246 ◽  
Author(s):  
Sunil Kumar ◽  
Priyanka Kumari ◽  
Shoma Devi
Keyword(s):  
Body Weight ◽  
Tissue Injury ◽  
Curcuma Longa ◽  
Fatty Infiltration ◽  
Rattus Rattus ◽  
Protective Role ◽  
Pharmaceutical Drugs ◽  
Urinary Hydroxyproline ◽  
Hydropic Degeneration

The purpose of this study was to know the hepatotoxicity of ethanol in laboratory rats Rattus rattus and to observe the individual and combined phytotherapeutic role of five herbs viz. Arctium lappa, Curcuma longa, Piper longum, Plumbago zeylanica and Terminalia chebula through biochemical and histopathological parameters. Ethanol is commonly used as solvent, pharmaceutical, drugs and alcohol abuse. Lipidperoxidation, glutathione content, urinary hydroxyproline, collagen and histopathological studies showed hepatotoxicity of 1 ml/kg bodyweight dose of ethanol and protective role of 100 mg/kg body weight dose of herbs. Histopathological changes observed in the liver of rats after ethanol treatment showed hepatitis, collagenesis, fatty infiltration, sclerosis, perilobular necrosis, cytoplasmic degeneration, enlarged bile canaliculi, hydropic degeneration, focal necrosis, binucleated hepatocytes and nuclear degeneration. Mild cytoplasmic degeneration, necrosis, collagenesis and hepatocytes regenerations were observed in rats treated with same dose of ethanol and herbal combination.Ethanol treatment decreased the glutathione content, increased tissue malondialdehyde and collagen content, thus causing tissue injury and liver collagenesis. Urinary hydroxyproline level and biochemical parameters also showed the protective role of herbs against ethanol induced toxicity. Herbal combination i. e. 100ml/kg body weight from the mixture of five herbs given orally was found more effective than their individual role. Herbs and plants contain aromatic substances, secondary metabolites, alkaloids and polyphenols which act as antioxidant thus showing protective role.

Protective role of Sterculia tragacantha aqueous extract on pancreatic gene expression and oxidative stress parameters in streptozotocin-induced diabetic rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Basiru Olaitan Ajiboye ◽  
Babatunji Emmanuel Oyinloye ◽  
Jennifer Chidera Awurum ◽  
Sunday Amos Onikanni ◽  
Adedotun Adefolalu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Protective Role ◽  
Diabetic Rats ◽  
Gene Expressions ◽  
Ki 67 ◽  
Oxidative Stress Parameters ◽  
And Oxidative Stress ◽  
Stress Parameters

Abstract Objectives The current study evaluates the protective role of aqueous extract of Sterculia tragacantha leaf (AESTL) on pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67 and GLP-1R) and oxidative stress parameters in streptozotocin-induced diabetic rats. Methods Diabetes mellitus was induced into the experimental Wistar animals via intraperitoneal (IP) injection of streptozotocin (35 mg/kg body weight) and 5% glucose water was given to the rats for 24 h after induction. The animals were categorized into five groups of 10 rats each as follows normal control, diabetic control, diabetic rats administered AESTL (150 and 300 mg/kg body weight) and diabetic rats administered metformin (200 mg/kg) orally for two weeks. Thereafter, the animals were euthanized, blood sample collected, pancreas harvested and some pancreatic gene expressions (such as insulin, PCNA, PDX-1, KI-67, and GLP-1R)s as well as oxidative stress parameters were analyzed. Results The results revealed that AESTL significantly (p<0.05) reduced fasting blood glucose level, food and water intake, and lipid peroxidation in diabetic rats. Diabetic rats administered different doses of AESTL showed a substantial upsurge in body weight, antioxidant enzyme activities, and pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67, and GLP-1R). Conclusions It can therefore be concluded that AESTL has the ability to protect the pancreas during diabetes mellitus conditions.

scholarly journals Protective role of ceftriaxone plus sulbactam with VRP1034 on oxidative stress, hematological and enzymatic parameters in cadmium toxicity induced rat model

2012 ◽  
Vol 5 (4) ◽  
pp. 192-200 ◽  
Author(s):  
Vivek Kumar Dwivedi ◽  
Anuj Bhatanagar ◽  
Manu Chaudhary
Keyword(s):  
Free Radical ◽  
Tissue Injury ◽  
Cadmium Toxicity ◽  
Treated Group ◽  
Protective Role ◽  
Enzymatic Activities ◽  
Exposed Group ◽  
Male Rats ◽  
Control Group

ABSTRACT We investigated the protective role of ceftriaxone plus sulbactam with VRP1034 (Elores) on hematological, lipid peroxidation, antioxidant enzymatic activities and Cd levels in the blood and tissues of cadmium exposed rats. Twenty-four male rats were divided into three groups of eight rats each. The control group received distilled water whereas group II received CdCl2 (1.5 mg/4 ml/body weight) through gastric gavage for 21 days. Group III received CdCl2 and was treated with ceftriaxone plus sulbactam with VRP1034 for 21 days. The hematological, biochemical, lipid per-oxidation levels and enzymatic parameters were measured in plasma and tissues (brain, liver and kidney) of all groups. The Cd, Zn and Fe levels were measured in blood and tissues of all groups. Our findings showed significantly decreased cadmium (p<0.001), malonaldialdehyde (p<0.001) and myloperoxidase (MPO) levels along with significantly increased hemoglobin (p<0.01), RBC (p<0.05), hematocrit (p<0.05) levels and all antioxidant enzymatic activities (SOD, CAT, GR, GPx) in plasma and tissues of ceftriaxone plus sulbactam with VRP1034 treated group as compared to cadmium exposed group. Delta aminolevulinate dehydratase (δ-ALAD) activity was significantly (p<0.001) increased in the blood of ceftriaxone plus sulbactam with VRP1034 treated group as compared with cadmium exposed group. The levels of hepatic and renal parameters were significantly (p<0.001) decreased in ceftriaxone plus sulbactam with VRP1034 treated group as compared to cadmium exposed group. These findings indicate that ceftriaxone plus sulbactam with VRP1034 acts as a potent free radical scavenger and exhibits metal chelating properties that reduce free radical mediated tissue injury and prevent dysfunction of hepatic and renal organs during metal intoxication.

PROTECTIVE ROLE OF HEME OXYGENASE 1 IN THE INTESTINAL TISSUE INJURY IN HEMORRHAGIC SHOCK IN RATS

Shock ◽  
2008 ◽  
Vol 29 (2) ◽  
pp. 252-261 ◽  
Author(s):  
Kazuyoshi Inoue ◽  
Toru Takahashi ◽  
Kenji Uehara ◽  
Hiroko Shimuzu ◽  
Kana Ido ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Heme Oxygenase ◽  
Tissue Injury ◽  
Protective Role ◽  
Heme Oxygenase 1 ◽  
Intestinal Tissue

scholarly journals PTX3 Regulation of Inflammation, Hemostatic Response, Tissue Repair, and Resolution of Fibrosis Favors a Role in Limiting Idiopathic Pulmonary Fibrosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Andrea Doni ◽  
Alberto Mantovani ◽  
Barbara Bottazzi ◽  
Remo Castro Russo
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Fibrosis ◽  
Tissue Repair ◽  
Therapeutic Potential ◽  
Tissue Injury ◽  
Life Quality ◽  
Unknown Origin ◽  
Protective Role

PTX3 is a soluble pattern recognition molecule (PRM) belonging to the humoral innate immune system, rapidly produced at inflammatory sites by phagocytes and stromal cells in response to infection or tissue injury. PTX3 interacts with microbial moieties and selected pathogens, with molecules of the complement and hemostatic systems, and with extracellular matrix (ECM) components. In wound sites, PTX3 interacts with fibrin and plasminogen and favors a timely removal of fibrin-rich ECM for an efficient tissue repair. Idiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive interstitial lung disease of unknown origin, associated with excessive ECM deposition affecting tissue architecture, with irreversible loss of lung function and impact on the patient’s life quality. Maccarinelli et al. recently demonstrated a protective role of PTX3 using the bleomycin (BLM)-induced experimental model of lung fibrosis, in line with the reported role of PTX3 in tissue repair. However, the mechanisms and therapeutic potential of PTX3 in IPF remained to be investigated. Herein, we provide new insights on the possible role of PTX3 in the development of IPF and BLM-induced lung fibrosis. In mice, PTX3-deficiency was associated with worsening of the disease and with impaired fibrin removal and subsequently increased collagen deposition. In IPF patients, microarray data indicated a down-regulation of PTX3 expression, thus suggesting a potential rational underlying the development of disease. Therefore, we provide new insights for considering PTX3 as a possible target molecule underlying therapeutic intervention in IPF.

Osthole Improves Acute Pancreatitis Injury by Regulating NF-κB, Nuclear Factor Pathway

2021 ◽  
Vol 19 (4) ◽  
pp. 532-536
Author(s):  
Shifeng Zhu ◽  
Xiaosheng Cai ◽  
Haicheng Dong ◽  
Bing Wang ◽  
Weixing Ying ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Tissue Injury ◽  
Inflammatory Cells ◽  
Protective Role ◽  
Pancreatic Acinar Cells ◽  
Caspase 9 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

We have investigated the protective role of osthole in tissue injury in experimentally induced acute pancreatitis in a rat model. Acute pancreatitis causes moderate to severe interstitial edema, extensive infiltration of inflammatory cells, marked vacuolation of pancreatic acinar cells, necrosis and hemorrhage in pancreatic tissues. Also, the levels of amylase and lipase, diagnostic markers of acute pancreatitis, are elevated with concurrent rise in the pro-inflammatory cytokinestumor necrosis factor-alpha, interleukin-6, and interleukin-1β. The levels of capase-3, caspase-9, cleaved-caspase-3 and cleaved-caspase-9 were also elevated. The phosphorylation of p65 and IκBα was upregulated and the expression of IκBα was downregulated. There was a diminution in all of the aforementioned changes following osthole administration. In conclusion, the results of this study demonstrated that osthole prevents tissue injury in acute pancreatitis through inhibition of the activation of NF-κB pathway, providing a new insight to potential treatment.

scholarly journals PROTECTIVE ACTIVITY OF ASPARAGUS RACEMOSUS IN METHOTREXATE-INDUCED LIVER TOXICITY IN WISTAR RATS

2018 ◽  
Vol 11 (9) ◽  
pp. 253
Author(s):  
Arul Daniel J ◽  
Susmita Das ◽  
Neethu Jayan ◽  
Asha Devi S
Keyword(s):  
Body Weight ◽  
Side Effects ◽  
Liver Toxicity ◽  
Protective Role ◽  
Hepatic Damage ◽  
Asparagus Racemosus ◽  
Group Iii ◽  
Group I ◽  
Group Ii

Objectives: Various clinically available drugs along with the beneficial action also have drastic side effects due to chronic exposure. In liver, these resulting side effects can be over production of reactive oxygen species, which will further lead to oxidative stress and hepatotoxicity. Therefore, as a preventive measure, the protective role of herbal extracts is being evaluated because of its high success rate and low toxic effects. The primary aim of this study was to evaluate the efficiency of the protective role of Asparagus racemosus is evaluated and studied against methotrexate (MTX)-induced hepatic damage in male Wistar albino rats.Methods: The course of the study was for 14 days. During this experimental study, the animals were categorized into four groups with six rats per group. Group I (positive control) which was treated with normal saline, Group II (negative control) with MTX 20 mg/kg of body weight on 12th day, Group III with A. racemosus 300 mg/kg of body weight + MTX 20 mg/kg on 12th day, and Group IV with A. racemosus 100 mg/kg of body weight + MTX 20 mg/kg on 12th day. On 14th day, the animals were sacrificed, and histopathological as well as antioxidant assays were performed.Results and Conclusion: Assays revealed high lipid peroxidation level and low antioxidant levels in Group II. Meanwhile, in Group III and IV, the levels were restored near to control, which supported the protective role of A. racemosus against MTX-induced hepatic damage. Histopathology evaluation also supported the above-mentioned findings.

scholarly journals Protective role of sildenafil citrate in isoniazid-rifampicin induced histomorphological changes in liver of albino mice

2021 ◽  
Vol 15 (1) ◽  
pp. 52-58
Author(s):  
Najma Hameed ◽  
Khalid Farooq
Keyword(s):  
Body Weight ◽  
Morphological Changes ◽  
Isotonic Saline ◽  
Daily Basis ◽  
Protective Role ◽  
Sildenafil Citrate ◽  
Control Group ◽  
Histomorphological Changes ◽  
Mice Liver

Objectives: The objective of the study was to reveal the reversal of histo-morphological changes in mice liver induced by combined isoniazid-rifampicin (INH-RIF) therapy with sildenafil treatment. Methods: Twenty-one mice weighing between 25–35 g were enrolled in the study. Randomisation was carried out by simple balloting method. The selected mice were sorted into three groups with 7 mice, each group. In group C (n=7) control group, mice were administered 0.4ml of saline per kg body weight daily intra peritoneally for 21 days. In group R (n=7) INH-RIF group, rifampicin (50 mg/kg) and isoniazid (50 mg/kg), dissolved in 4 ml/kg isotonic saline, were administered intra-peritoneally (ip) daily for 21 days. In group S (n=7) sildenafil administered group, 10 mg/kg sildenafil was given orally by gastric gavage on daily basis along with the intraperitoneal injection of INH-RIF (50 mg/kg each) daily for 21 days. Results: Histopathology revealed hepatotoxicity in group R (INH-RIF), while significant improvement was observed in group C (INH-RIF-sildenafil). Conclusion: Sildenafil citrate possesses hepatoprotective role against INH-RIF induced hepatotoxicity.

scholarly journals Interleukin-9 in Immunopathology of Trypanosoma cruzi Experimental Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Nadjania Saraiva de Lira Silva ◽  
Cristina Mary Orikaza ◽  
Fabiana Rodrigues de Santana ◽  
Luana Aguiar dos Santos ◽  
Bruno Ramos Salu ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Experimental Infection ◽  
Cardiac Fibrosis ◽  
Tissue Injury ◽  
Chronic Phase ◽  
Protective Role

Chagas’ disease is a parasitosis caused by Trypanosoma cruzi, which affects approximately 8 million people worldwide. The balance between pro- and anti-inflammatory cytokines produced during immunological responses contributes to disease prognosis and progression. Parasite tissue persistence can induce chronic inflammatory stimuli, which can cause long-term tissue injury and fibrosis. Chronic Chagas’ patients exhibit increased levels of interleukin (IL)-9, an important cytokine in the regulation of inflammatory and fibrogenic processes. Data on the role of IL-9 in other pathologies are sometimes contradictory, and few studies have explored this cytokine’s influence in Chagas’ disease pathology. Hence, the aim of this study was to evaluate the role of IL-9 in the progression of T. cruzi infection in vivo and in vitro. In vitro infection demonstrated that IL-9 reduced the number of infected cells and decreased the multiplication of intracellular amastigotes in both C2C12 myoblasts and bone marrow-derived macrophages. In myoblasts, the increased production of nitric oxide (NO) was essential for reduced parasite multiplication, whereas macrophage responses resulted in increased IL-6 and reduced TGF-β levels, indicating that parasite growth restriction mechanisms induced by IL-9 were cell-type specific. Experimental infection of BALB/c mice with T. cruzi trypomastigotes of the Y strain implicated a major role of IL-9 during the chronic phase, as increased Th9 and Tc9 cells were detected among splenocytes; higher levels of IL-9 in these cell populations and increased cardiac IL-9 levels were detected compared to those of uninfected mice. Moreover, rIL9 treatment decreased serum IL-12, IL-6, and IL-10 levels and cardiac TNF-α levels, possibly attempting to control the inflammatory response. IL-9 neutralization increased cardiac fibrosis, synthesis of collagens I and III, and mastocyte recruitment in BALB/c heart tissue during the chronic phase. In conclusion, our data showed that IL-9 reduced the invasion and multiplication of T. cruzi in vitro, in both myoblasts and macrophages, favoring disease control through cell-specific mechanisms. In vivo, IL-9 was elevated during experimental chronic infection in BALB/c mice, and this cytokine played a protective role in the immunopathological response during this phase by controlling cardiac fibrosis and proinflammatory cytokine production.

scholarly journals ACE2: from protection of liver disease to propagation of COVID-19

2020 ◽  
Vol 134 (23) ◽  
pp. 3137-3158 ◽  
Author(s):  
Fiona J. Warner ◽  
Harinda Rajapaksha ◽  
Nicholas Shackel ◽  
Chandana B. Herath
Keyword(s):  
Liver Disease ◽  
Tissue Injury ◽  
Renin Angiotensin System ◽  
Protective Role ◽  
Alveolar Epithelial Cells ◽  
Cellular Receptor ◽  
Alveolar Epithelial ◽  
Key Enzyme ◽  
Life Threatening

Abstract Twenty years ago, the discovery of angiotensin-converting enzyme 2 (ACE2) was an important breakthrough dramatically enhancing our understanding of the renin–angiotensin system (RAS). The classical RAS is driven by its key enzyme ACE and is pivotal in the regulation of blood pressure and fluid homeostasis. More recently, it has been recognised that the protective RAS regulated by ACE2 counterbalances many of the deleterious effects of the classical RAS. Studies in murine models demonstrated that manipulating the protective RAS can dramatically alter many diseases including liver disease. Liver-specific overexpression of ACE2 in mice with liver fibrosis has proved to be highly effective in antagonising liver injury and fibrosis progression. Importantly, despite its highly protective role in disease pathogenesis, ACE2 is hijacked by SARS-CoV-2 as a cellular receptor to gain entry to alveolar epithelial cells, causing COVID-19, a severe respiratory disease in humans. COVID-19 is frequently life-threatening especially in elderly or people with other medical conditions. As an unprecedented number of COVID-19 patients have been affected globally, there is an urgent need to discover novel therapeutics targeting the interaction between the SARS-CoV-2 spike protein and ACE2. Understanding the role of ACE2 in physiology, pathobiology and as a cellular receptor for SARS-CoV-2 infection provides insight into potential new therapeutic strategies aiming to prevent SARS-CoV-2 infection related tissue injury. This review outlines the role of the RAS with a strong focus on ACE2-driven protective RAS in liver disease and provides therapeutic approaches to develop strategies to prevent SARS-CoV-2 infection in humans.

scholarly journals Protective role of spleen-derived macrophages in lung inflammation, injury, and fibrosis induced by nitrogen mustard

2015 ◽  
Vol 309 (12) ◽  
pp. L1487-L1498 ◽  
Author(s):  
Alessandro Venosa ◽  
Rama Malaviya ◽  
Andrew J. Gow ◽  
Leroy Hall ◽  
Jeffrey D. Laskin ◽  
...  
Keyword(s):  
Nitrogen Mustard ◽  
Tissue Injury ◽  
Protective Role ◽  
M2 Macrophages ◽  
Targeted Therapeutics ◽  
Sham Control ◽  
M1 Macrophages ◽  
Lung Macrophages ◽  
Cox 2

Nitrogen mustard (NM) is a vesicant that causes lung injury and fibrosis, accompanied by a persistent macrophage inflammatory response. In these studies we analyzed the spleen as a source of these cells. Splenectomized (SPX) and sham control rats were treated intratracheally with NM (0.125 mg/kg) or PBS control. Macrophage responses were analyzed 1–7 days later. Splenectomy resulted in an increase in lung macrophages expressing CCR2, but a decrease in ATR-1α+ cells, receptors important in bone marrow and spleen monocyte trafficking, respectively. Splenectomy was also associated with an increase in proinflammatory M1 (iNOS+, CD11b+CD43+) macrophages in lungs of NM-treated rats, as well as greater upregulation of iNOS and COX-2 mRNA expression. Conversely, a decrease in CD11b+CD43− M2 macrophages was observed in SPX rats, with no changes in CD68+, CD163+, CD206+, or YM-1+ M2 macrophages, suggesting distinct origins of M2 subpopulations responding to NM. Macrophage expression of M2 genes including IL-10, ApoE, PTX-2, PTX-3, 5-HT2α, and 5-HT7 was also reduced in NM-treated SPX rats compared with shams, indicating impaired M2 activity. Changes in lung macrophages responding to NM as a consequence of splenectomy were correlated with exacerbated tissue injury and more rapid fibrogenesis. These data demonstrate that the spleen is a source of a subset of M2 macrophages with anti-inflammatory activity; moreover, in their absence, proinflammatory/cytotoxic M1 macrophages predominate in the lung, resulting in heightened pathology. Understanding the origin of macrophages and characterizing their phenotype after vesicant exposure may lead to more targeted therapeutics aimed at reducing toxicity and disease pathogenesis.

Sign in / Sign up

Export Citation Format

Share Document