scholarly journals Protective role of methanol extracts of Gentiana asclepiadea L. and G. cruciata L. against genotoxic damage induced by ethyl methanesulfonate

Genetika ◽  
2013 ◽  
Vol 45 (2) ◽  
pp. 329-340 ◽  
Author(s):  
Sanja Matic ◽  
Snezana Stanic ◽  
Slavica Solujic ◽  
Nevena Stankovic ◽  
Milan Mladenovic ◽  
...  
Keyword(s):  
Aerial Part ◽  
Protective Role ◽  
Negative Control ◽  
Ethyl Methanesulfonate ◽  
Recessive Lethal ◽  
Methanol Extracts ◽  
Strong Mutagen ◽  
Gentiana Cruciata

The methanol extracts from the underground and aerial part of the two species of Gentiana genus, Gentiana asclepiadea L. and Gentiana cruciata L. from Serbia, were investigated for their antigenotoxic activity against wellestablished mutagenic agent ethyl methanesulfonate (EMS) using the in vivo sexlinked recessive lethal (SLRL) test on Drosophila melanogaster. For this purpose, three days old Canton S males were treated with the potent mutagen EMS in concentration of 0.75 ppm, alone and combined with methanol extracts obtained from underground or aerial part of G. asclepiadea and G. cruciata in concentration of 5%, separately. Although EMS in concentration of 0.75 ppm increased the mutation frequency in all three broods, post-treatments with methanol extracts obtained from the underground and aerial part of G. asclepiadea and G. cruciata in concentration of 5%, respectively, drastically reduced the frequency of sex-linked recessive lethal mutations induced by EMS. Compared to the sucrose, as a negative control, methanol extract obtained from underground part of G. cruciata showed the most potent antigenotoxic activity. Extracts from the underground and aerial part of the two species of Gentiana genus, G. asclepiadea L. and G. cruciata L. from Serbia used in our experiments showed a clear antimutagenic effect, reducing the frequency of mutations induced by a strong mutagen such as EMS.

scholarly journals THE PROTECTIVE ROLE OF OMEGA-3 AGAINST GENOTOXICITY AND REPRODUCTIVE TOXICITY OF COBALT OXIDE NANOPARTICLES ACUTE TREATMENT IN MALE MICE

2018 ◽  
Vol 11 (5) ◽  
pp. 423
Author(s):  
Nahed A Hussien ◽  
Hanan R. H. Mohamed
Keyword(s):  
Cobalt Oxide ◽  
Negative Control Group ◽  
Protective Role ◽  
Negative Control ◽  
Control Group ◽  
Omega 3 ◽  
Genotoxic Potential ◽  
Polychromatic Erythrocytes

Objective: Cobalt nanoparticles (NPs), especially cobalt oxide NPs (Co3O4 NPs) are attracting unique shaped NPs that are used in different biomedical applications and medicine. Different in vitro studies report their toxic and carcinogenic effect but limited in vivo studies were present on its genotoxic potential. The present study was aimed to evaluate the genotoxic potential of Co3O4 NPs on bone marrow cells and sperms and the protective role of omega-3 in male albino mice.Methods: Animals were segregated into four groups that were orally treated for 3 consecutive days, Group 1: Negative control; Group 2: Omega-3 (250 mg/kg); Group 3: Co3O4 NPs (20 mg/kg); and Group 4: Combined group (250 mg/kg Omega-3 and Co3O4 NPs 20 mg/kg).Results: The present results show that Co3O4 NPs administration significantly increased number of micronucleated polychromatic erythrocytes (PCEs)/1000 PCEs, sperm abnormalities, and DNA damage, significantly decreased sperm motility and concentration in comparison to negative control group. However, Omega-3 administration in the combined group modulates the genotoxic potential of Co3O4 NPs in comparison to Co3O4 NPs group.Conclusion: The present study reports the genotoxic potential of Co3O4 NPs in vivo and assesses the protective role of Omega-3 administration due to its antioxidant effect.

scholarly journals A neuroprotective role for microglia in prion diseases

2016 ◽  
Vol 213 (6) ◽  
pp. 1047-1059 ◽  
Author(s):  
Caihong Zhu ◽  
Uli S. Herrmann ◽  
Jeppe Falsig ◽  
Irina Abakumova ◽  
Mario Nuvolone ◽  
...  
Keyword(s):  
Prion Diseases ◽  
Protective Role ◽  
Proteinase K ◽  
Immune Effector ◽  
Effector Cells ◽  
The Central Nervous System ◽  
Cultured Slices ◽  
Simplex Virus

Microglial activation is a hallmark of most neurodegenerative disorders, and is particularly conspicuous in prion diseases. However, the role of microglia, which function as both primary immune effector cells and professional phagocytes in the central nervous system, remains contentious in the context of neurodegeneration. Here, we evaluated the effect of microglial depletion/deficiency on prion pathogenesis. We found that ganciclovir-mediated microglial ablation on tga20/CD11b-thymidine kinase of Herpes simplex virus (HSVTK) cerebellar organotypic cultured slices markedly aggravated prion-induced neurotoxicity. A similar deterioration of disease was recapitulated in in vivo microglial depletion in prion-infected tga20/CD11b-HSVTK mice. Additionally, deficiency of microglia in interleukin 34 knockout (IL34−/−) mice again resulted in significantly augmented proteinase K–resistant prion protein deposition and accelerated prion disease progression. These results provide unambiguous evidence for a general protective role of microglia in prion pathogenesis.

scholarly journals A Protective Role of Paeoniflorin in Fluctuant Hyperglycemia-Induced Vascular Endothelial Injuries through Antioxidative and Anti-Inflammatory Effects and Reduction of PKCβ1

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jing-Shang Wang ◽  
Ye Huang ◽  
Shuping Zhang ◽  
Hui-Jun Yin ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Level ◽  
Umbilical Vein ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Glucose Levels ◽  
Umbilical Vein Endothelial Cells

Hyperglycemia fluctuation is associated with diabetes mellitus (DM) complications when compared to persistent hyperglycemia. Previous studies have shown that paeoniflorin (PF), through its antiapoptosis, anti-inflammation, and antithrombotic properties, effectively protects against cardiovascular and cerebrovascular disease. However, the mechanism underlying the protection from PF against vascular injuries induced by hyperglycemia fluctuations remains poorly understood. Herein, we investigated the potential protective role of PF on human umbilical vein endothelial cells (HUVECs) subjected to intermittent glucose levels in vitro and in DM rats with fluctuating hyperglycemia in vivo. A remarkable increased apoptosis associated with elevated inflammation, increased oxidative stress, and high protein level of PKCβ1 was induced in HUVECs by intermittently changing glucose for 8 days, and PF recovered those detrimental changes. LY333531, a potent PKCβ1 inhibitor, and metformin manifested similar effects. Additionally, in DM rats with fluctuating hyperglycemia, PF protected against vascular damage as what has been observed in vitro. Taken together, PF attenuates the vascular injury induced by fluctuant hyperglycemia through oxidative stress inhibition, inflammatory reaction reduction, and PKCβ1 protein level repression, suggesting its perspective clinical usage.

scholarly journals Impact of GPR1 signaling on maternal high-fat feeding and placenta metabolism in mice

2019 ◽  
Vol 316 (6) ◽  
pp. E987-E997 ◽  
Author(s):  
Binbin Huang ◽  
Chen Huang ◽  
Huashan Zhao ◽  
Wen Zhu ◽  
Baobei Wang ◽  
...  
Keyword(s):  
Biological Effects ◽  
Negative Control ◽  
Feedback Mechanism ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Maternal Metabolism ◽  
Phosphorylated Akt

Chemerin and G protein-coupled receptor 1 (GPR1) are increased in serum and placenta in mice during pregnancy. Interestingly, we observed increased serum chemerin levels and decreased GPR1 expression in placenta of high-fat-diet-fed mice compared with chow-fed mice at gestational day 18. GPR1 protein and gene levels were significantly decreased in gestational diabetes mellitus (GDM) patient placentas. Therefore, we hypothesized that chemerin/GPR1 signaling might participate in the pathogenic mechanism of GDM. We investigated the role of GPR1 in carbohydrate homeostasis during pregnancy using pregnant mice transfected with small interfering RNA for GPR1 or a negative control. GPR1 knockdown exacerbated glucose intolerance, disrupted lipid metabolism, and decreased β-cell proliferation and insulin levels. Glucose transport protein-3 and fatty acid binding protein-4 were downregulated with reducing GPR1 in vivo and in vitro via phosphorylated AKT pathway. Taken together, our findings first demonstrate the expression of GPR1, the characterization of its direct biological effects in humans and mice, as well as the molecular mechanism that indicates the role of GPR1 signaling in maternal metabolism during pregnancy, suggesting a novel feedback mechanism to regulate glucose balance during pregnancy, and GPR1 could be a potential target for the detection and therapy of GDM.

scholarly journals HDAC2 attenuates airway inflammation by suppressing IL-17A production in HDM-challenged mice

2019 ◽  
Vol 316 (1) ◽  
pp. L269-L279 ◽  
Author(s):  
Tianwen Lai ◽  
Mindan Wu ◽  
Chao Zhang ◽  
Luanqing Che ◽  
Feng Xu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Inflammatory Cells ◽  
Protective Role ◽  
In Vivo Models

Histone deacetylase (HDAC)2 is expressed in airway epithelium and plays a pivotal role in inflammatory cells. However, the role of HDAC2 in allergic airway inflammation remains poorly understood. In the present study, we determined the role of HDAC2 in airway inflammation using in vivo models of house dust mite (HDM)-induced allergic inflammation and in vitro cultures of human bronchial epithelial (HBE) cells exposed to HDM, IL-17A, or both. We observed that HDM-challenged Hdac2+/− mice exhibited substantially enhanced infiltration of inflammatory cells. Higher levels of T helper 2 cytokines and IL-17A expression were found in lung tissues of HDM-challenged Hdac2+/− mice. Interestingly, IL-17A deletion or anti-IL-17A treatment reversed the enhanced airway inflammation induced by HDAC2 impairment. In vitro, HDM and IL-17A synergistically decreased HDAC2 expression in HBE cells. HDAC2 gene silencing further enhanced HDM- and/or IL-17A-induced inflammatory cytokines in HBE cells. HDAC2 overexpresion or blocking IL-17A gene expression restored the enhanced inflammatory cytokines. Collectively, these results support a protective role of HDAC2 in HDM-induced airway inflammation by suppressing IL-17A production and might suggest that activation of HDAC2 and/or inhibition of IL-17A production could prevent the development of allergic airway inflammation.

scholarly journals Role of nitric oxide in hepatic microvascular injury elicited by acetaminophen in mice

2004 ◽  
Vol 286 (1) ◽  
pp. G60-G67 ◽  
Author(s):  
Yoshiya Ito ◽  
Edward R. Abril ◽  
Nancy W. Bethea ◽  
Robert S. McCuskey
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Cell Injury ◽  
Parenchymal Cell ◽  
Protective Role ◽  
Hepatic Expression ◽  
Inos Inhibitor ◽  
Microcirculatory Disturbances

Nitric oxide (NO) is suggested to play a role in liver injury elicited by acetaminophen (APAP). Hepatic microcirculatory dysfunction also is reported to contribute to the development of the injury. As a result, the role of NO in hepatic microcirculatory alterations in response to APAP was examined in mice by in vivo microscopy. A selective inducible NO synthase (iNOS) inhibitor,l- N6-(1-iminoethyl)-lysine (l-NIL), or a nonselective NOS inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), was intraperitoneally administered to animals 10 min before APAP gavage. l-NIL suppressed raised alanine aminotransferase (ALT) values 6 h after APAP, whereas l-NAME increased those 1.7-fold. Increased ALT levels were associated with hepatic expression of iNOS. l-NIL, but not l-NAME, reduced the expression. APAP caused a reduction (20%) in the numbers of perfused sinusoids. l-NIL restored the sinusoidal perfusion, but l-NAME was ineffective. APAP increased the area occupied by infiltrated erythrocytes into the extrasinusoidal space. l-NIL tended to minimize this infiltration, whereas l-NAME further enhanced it. APAP caused an increase (1.5-fold) in Kupffer cell phagocytic activity. This activity in response to APAP was blunted by l-NIL, whereas l-NAME further elevated it. l-NIL suppressed APAP-induced decreases in hepatic glutathione levels. These results suggest that NO derived from iNOS contributes to APAP-induced parenchymal cell injury and hepatic microcirculatory disturbances. l-NIL exerts preventive effects on the liver injury partly by inhibiting APAP bioactivation. In contrast, NO derived from constitutive isoforms of NOS exerts a protective role in liver microcirculation against APAP intoxication and thereby minimizes liver injury.

Protective role of Mycobacterium leprae small heat-shock protein in heterologous hosts, Escherichia coli and Mycobacterium smegmatis, grown under stress

2013 ◽  
Vol 62 (7) ◽  
pp. 959-967 ◽  
Author(s):  
Jayapal Jeya Maheshwari ◽  
Kuppamuthu Dharmalingam
Keyword(s):  
Escherichia Coli ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Mycobacterium Smegmatis ◽  
Small Heat Shock Protein ◽  
Mycobacterium Leprae ◽  
Protective Role ◽  
Low Oxygen

The aim of this study is to examine the in vivo role of a small heat-shock protein (sHsp18) from Mycobacterium leprae in the survival of heterologous recombinant hosts carrying the gene encoding this protein under different environmental conditions that are normally encountered by M. leprae during its infection of the human host. Using an Escherichia coli system where shsp18 expression is controlled by its native promoter, we show that expression of shsp18 is induced under low oxygen tension, nutrient depletion and oxidative stress, all of which reflect the natural internal environment of the granulomas where the pathogen resides for long periods. We demonstrate the in vivo chaperone activity of sHsp18 through its ability to confer survival advantage to recombinant E. coli at heat-shock temperatures. Additional evidence for the protective role of sHsp18 was obtained when Mycobacterium smegmatis harbouring a copy of shsp18 was found to multiply better in human macrophages. Furthermore, the autokinase activity of sHsp18 protein demonstrated for what is believed to be the first time in this study implies that some of the functions of sHsp18 might be controlled by the phosphorylation state of this protein. Results from this study suggest that shsp18 might be one of the factors that facilitate the survival and persistence of M. leprae under stress and autophosphorylation of sHsp18 protein could be a mechanism used by this protein to sense changes in the external environment.

Protective role of NO in hepatic microcirculatory dysfunction during endotoxemia

1994 ◽  
Vol 267 (6) ◽  
pp. G1135-G1141 ◽  
Author(s):  
J. Nishida ◽  
R. S. McCuskey ◽  
D. McDonnell ◽  
E. S. Fox
Keyword(s):  
Hepatic Injury ◽  
Protective Role ◽  
No Production ◽  
Leukocyte Adherence ◽  
In Vivo Microscopy ◽  
Hepatic Microcirculation ◽  
Protective Function ◽  
Microcirculatory Disturbances

Nitric oxide (NO) has been reported to have a protective function in attenuating hepatic injury during endotoxemia or sepsis. As a result, the role of NO in attenuating the hepatic microcirculatory alterations associated with endotoxemia was investigated in mice by in vivo microscopy. The livers were examined 2 h after intravenous injection of Escherichia coli 0111:B4 lipopolysaccharide (LPS) alone or in combination with inhibitors of the synthesis of NO, NG-nitro-L-arginine methyl ester or NG-monomethyl-L-arginine. In the animals treated with the combination of NO synthase inhibitors and LPS, leukocyte adherence was increased threefold above that in animals treated with LPS alone. This was accompanied by a 33% reduction in sinusoidal blood flow. Simultaneous administration of L-arginine, but not D-arginine, eliminated these microcirculatory disturbances. The results demonstrate that inhibition of LPS-stimulated NO production results in an early hepatic microvascular inflammatory response to a dose of endotoxin which by itself is scarcely inflammatory. This suggests that NO plays a significant role in stabilizing the hepatic microcirculation during endotoxemia, thereby helping to protect the liver from ischemia and leukocyte-induced oxidative injury.

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