scholarly journals Protective Effect of Alamandine on Doxorubicin‑Induced Nephrotoxicity in Rats

2021 ◽  
Author(s):  
Ava Soltani Hekmat ◽  
Ameneh Chenari ◽  
Hiva Alipanah ◽  
Kazem Javanmardi
Keyword(s):  
Transcription Factor ◽  
Protective Effect ◽  
Water Intake ◽  
Immunohistochemical Analysis ◽  
Treated Group ◽  
The Other ◽  
Protective Effects ◽  
Osmotic Pumps ◽  
Immunohistochemical Studies ◽  
Gpx Activity

Abstract Background: The objective of this study was to evaluate the protective effects of alamandine, a new member of the angiotensin family, against doxorubicin (DOX)-induced nephrotoxicity in rats.Methods: Rats, intraperitoneally injected with DOX (3.750 mg/kg/week) to reach total cumulative dose of 15 mg/kg on day 35. Alamandine (50µg/kg/day) was administered to the rats via mini-osmotic pumps for 42 days. At the end of experiment, rats were placed in the metabolic cages for 24 h for measurement of water intake and urine output. After scarification, Serum and kidney tissues were collected, and biochemical, histopathological and immunohistochemical studies were carried out.Results: Inflammatory cytokines (IL-1β, IL-6), pro-fibrotic mediator (TGF-β), pro-inflammatory transcription factor (NF-kB), renal MDA, creatinine clearance, BUN, and water intake were increased by DOX administration. On the other hand, renal SOD, renal GPx activity and urinary output were decreased in the DOX-treated group. Alamandine co-therapy decreased these effects, as confirmed by histopathology and immunohistochemical analysisConclusion: The results of this study suggest that alamandine has the potential in preventing the nephrotoxicity induced by DXR in rats.

scholarly journals Protective effect of alamandine on doxorubicin‑induced nephrotoxicity in rats

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ava Soltani Hekmat ◽  
Ameneh Chenari ◽  
Hiva Alipanah ◽  
Kazem Javanmardi
Keyword(s):  
Water Intake ◽  
Transforming Growth Factor ◽  
Immunohistochemical Analysis ◽  
Transforming Growth Factor Β ◽  
Treated Group ◽  
Protective Effects ◽  
Osmotic Pumps ◽  
Immunohistochemical Studies ◽  
Gpx Activity ◽  
Pro Inflammatory Cytokines

Abstract Background This study aimed to evaluate the protective effects of alamandine, a new member of the angiotensin family, against doxorubicin (DOX)-induced nephrotoxicity in rats. Methods Rats were intraperitoneally injected with DOX (3.750 mg/kg/week) to reach a total cumulative dose of 15 mg/kg by day 35. Alamandine (50 µg/kg/day) was administered to the rats via mini-osmotic pumps for 42 days. At the end of the experiment, rats were placed in the metabolic cages for 24 h so that their water intake and urine output could be measured. After scarification, the rats’ serum and kidney tissues were collected, and biochemical, histopathological, and immunohistochemical studies were carried out. Results DOX administration yielded increases in pro-inflammatory cytokines, including interleukin (IL)-1β and IL-6, pro-fibrotic proteins transforming growth factor-β (TGF-β), pro-inflammatory transcription factor nuclear kappa B (NF-κB), kidney malondialdehyde (MDA), creatinine clearance, blood urea nitrogen (BUN), and water intake. On the other hand, the DOX-treated group exhibited decreased renal superoxide dismutase (SOD), renal glutathione peroxidase (GPx) activity, and urinary output. Alamandine co-therapy decreased these effects, as confirmed by histopathology and immunohistochemical analysis. Conclusions The results suggest that alamandine can prevent nephrotoxicity induced by DOX‎ in rats.

scholarly journals Protective Effects of Gymnema inodorum Leaf Extract on Plasmodium berghei-Induced Hypoglycemia, Dyslipidemia, Liver Damage, and Acute Kidney Injury in Experimental Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Kongsak Boonyapranai ◽  
Sirirat Surinkaew ◽  
Voravuth Somsak ◽  
Rujikorn Rattanatham
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Liver Damage ◽  
Biological Markers ◽  
Plasmodium Berghei ◽  
Leaf Extract ◽  
Kidney Injury ◽  
Treated Group ◽  
Therapeutic Effects ◽  
Protective Effects

Malaria complications are the most frequent cause of mortality from parasite infection. This study is aimed at investigating the protective effect of Gymnema inodorum leaf extract (GIE) on hypoglycemia, dyslipidemia, liver damage, and acute kidney injury induced by Plasmodium berghei infection in mice. Groups of ICR mice were inoculated with 1 × 10 7 parasitized erythrocytes of P. berghei ANKA and administered orally by gavage with 100, 250, and 500 mg/kg of GIE for 4 consecutive days. Healthy and untreated controls were given distilled water, while the positive control was treated with 10 mg/kg of chloroquine. The results showed that malaria-associated hypoglycemia, dyslipidemia, liver damage, and acute kidney injury were found in the untreated mice as indicated by the significant alteration of biological markers. On the contrary, in 250 and 500 mg/kg of GIE-treated mice, the biological markers were normal compared to healthy controls. The highest protective effect was found at 500 mg/kg similar to the CQ-treated group. However, GIE at a dose of 100 mg/kg did not show protection during malaria infection. This study demonstrated that GIE presented potential therapeutic effects on PbANKA-induced hypoglycemia, dyslipidemia, liver damage, and acute kidney injury. The results obtained confirm the prospect of G. inodorum as an essential source of new antimalarial compounds and justify folkloric use as an alternative malarial treatment.

scholarly journals The Protective Effects of Shen-Fu Injection on Experimental Acute Pancreatitis in a Rat Model

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Lei Huang ◽  
Jun Cao
Keyword(s):  
Oxidative Stress ◽  
Acute Pancreatitis ◽  
Nuclear Factor Kappa B ◽  
Treated Group ◽  
The Other ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Experimental Acute Pancreatitis ◽  
Histopathological Studies ◽  
Biochemical Indices

Objectives. In the present study, we investigated the protective effects of Shen-Fu injection (SFI) on a caerulein-induced rat pancreatitis (AP) model.Methods. SFI was given to rats in the SFI treated group through intraperitoneal injection. Blood and pancreas samples were collected for serological and histopathological studies.Results. Our results showed that AP caused significant decrease in tissue glutathione (GSH) and serum IL-4 and IL-10, while pancreatic malondialdehyde (MDA) and myeloperoxidase (MPO) were increased. Furthermore, TNF-α, IL-1β, amylase, and lipase levels were also significantly increased. On the other hand, SFI treatment reserved all these biochemical indices as well as histopathologic alterations that were induced by caerulein.Conclusion. Our findings suggest that the SFI protects against caerulein-induced AP in rats via modulation of cytokines, oxidative stress, and Nuclear Factor-kappa B (NF-κB) activity.

scholarly journals Redox Nanoparticle Therapeutics for Acetaminophen-Induced Hepatotoxicity in Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Phetcharat Boonruamkaew ◽  
Pennapa Chonpathompikunlert ◽  
Yukio Nagasaki
Keyword(s):  
Prothrombin Time ◽  
Histopathological Examination ◽  
Treated Group ◽  
The Other ◽  
Control Group ◽  
Activity Inhibition ◽  
Redox Nanoparticle ◽  
Histological Staining ◽  
Gpx Activity ◽  
Alt Activity

The purpose of this study was to evaluate the hepatoprotective effect of an antioxidative nanoparticle (RNPN) recently developed against APAP-induced hepatotoxicity in mice. The effects of oral administration ofRNPNto APAP-treated mice were assessed for various biochemical liver function parameters: alanine transaminase (ALT) activity, aspartate transaminase (AST) activity, alkaline phosphatase (ALP) activity, prothrombin time, and serum albumin (ALB) level. The treatment effects were assessed in terms of free radical parameters: malondialdehyde (MDA) accumulation, glutathione peroxidase (GPx) activity, % inhibition of superoxide anion (O2-∙), and histopathological examination. TheN-acetylcysteine (NAC)-treated group exhibited an enhanced prothrombin time relative to the control group, whileRNPNdid not prolong prothrombin time. TheRNPN-treated animals exhibited lower levels of ALT, AST, and ALP, while increased ALB levels were measured in these animals compared to those in the other groups. TheRNPN-treated animals furthermore exhibited improved MDA levels, GPx activity, and % inhibition ofO2-∙, which relate to oxidative damage. Histological staining of liver tissues fromRNPN-treated animals did not reveal any microscopic changes relative to the other groups. The findings of this study suggest thatRNPNpossesses effective hepatoprotective properties and does not exhibit the notable adverse effects associated with NAC treatment.

Protective Effect of Algerian Genista vepres Pomel Plant Against Isoniazid and Rifampicin Induced Liver Injury in Wistar Albino Rats

2021 ◽  
Vol 17 ◽  
Author(s):  
Lamia Zehani ◽  
Wafa Kerkatou ◽  
Souad Hamdouche ◽  
Somia Lassed ◽  
Ouahiba Boumaza ◽  
...  
Keyword(s):  
Vitamin E ◽  
Liver Injury ◽  
Protective Effect ◽  
Liver Tissue ◽  
Hepatic Dysfunction ◽  
Treated Group ◽  
Albino Rats ◽  
Wistar Albino Rats ◽  
Histopathological Studies ◽  
Gpx Activity

Background: The aim of the present study is to evaluate the protective effect of n-BuOH fraction of Genista vepres Pomel and Vitamin E against Isoniazid and Rifampicin (INH-RIF)-induced liver injury. Methods: Male Wistar Albino rats were dividing into eight equal groups treated with plant fraction (50 mg/kg, 100 mg/kg), vitamin E (100 mg/kg) and INH-RIF (100 mg/kg body weight /day each). At the end of the experiment, animals dissected and samples (blood, liver tissue) were removed and isolated for biochemical and histological studies. Results : Administration of INH-RIF for 21 days resulted in hepatic failure as evidenced by the elevation of biochemical parameters levels, and hepatic oxidative stress, which was associated with extensive hepatic parenchyma alteration. The pretreatment of the rat with G. vepres Pomel attenuated the increase of hepatic dysfunction markers, decreased significantly the level of malondialdehyde (MDA). Increased GSH level, GPx and catalase activities compared to INH-RIF treated group. However, the Vitamin E co-treatment decreased MDA level and increased GPx activity but did not show any effect in catalase or GSH parameters. The histopathological studies in the liver of rats also supported that both plant fraction and vitamin E markedly reduced the toxicity of INH-RIF and preserved the histoarchitecture of liver tissue. Conclusion: The results suggested that the n-BuOH fraction of G. vepres Pomel acts as a potent hepatoprotective agent against INH-RIF induced Hepatic dysfunction in rats.

scholarly journals Protective effect of leaf extract of Ficus carica L. against carbon tetrachloride-induced hepatic toxicity in mice and HepG2 cell line

2021 ◽  
Vol 20 (1) ◽  
pp. 113-119
Author(s):  
Syeda Hira ◽  
Muhammad Gulfraz ◽  
S.M. Saqlan Naqvi ◽  
Rehmat Ullah Qureshi ◽  
Hina Gul
Keyword(s):  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Hepg2 Cell ◽  
Leaf Extract ◽  
Treated Group ◽  
Ficus Carica ◽  
Protective Effects ◽  
Hepatoprotective Effects

Purpose: To determine the in vivo and in vitro hepatoprotective effects of Ficus carica.Methods: The methanol leaf extract of Ficus carica L was further fractionated into n-hexane, ethyl acetate and aqueous fractions. For in vivo study, male albino mice were divided into twelve groups. Hepatotoxicity was induced in the mice using carbon tetrachloride (CCl4). The extract of F. carica and its fractions were administered at doses of 200 and 400 mg/kg. Silymarin was used as standardhepatoprotective drug. The protective effects of the extract and fractions were determined via assay of biochemical parameters and antioxidant enzymes in the liver. The histopathology of the liver was also studied. Moreover, the in vitro hepatoprotective effect of the extract and fractions against CCl4-induced damage was determined in HepG2 cell line.Results: There were significant increases in the serum levels of liver biomarkers in CCl4-treated group, whereas treatments with plant extract and fractions significantly reduced the levels of these parameters (p < 0.05). In addition, results from histopathology revealed evidence of protective effect of Ficus carica through reversal of CCl4-induced decreases in the activities of liver antioxidant enzymes.Conclusion: These results indicate that methanol leaf extract of Ficus carica L. and its fractions exert significant and dose-dependent hepatoprotective effects in vivo and in vitro. Keywords: Ficus carica, Hepatoprotection, Carbon tetrachloride, Liver biomarkers

Effect of prolactin inhibition under heat exposure on water intake and excretion of urine, sodium and potassium in bulls

1980 ◽  
Vol 94 (3) ◽  
pp. 315-320 ◽  
Author(s):  
D. Schams ◽  
E. Stephan ◽  
R. D. Hooley
Keyword(s):  
Water Intake ◽  
Heat Exposure ◽  
Physiological Role ◽  
Treated Group ◽  
Serum Prolactin ◽  
Control Value ◽  
Light Regimen ◽  
Group I ◽  
Urinary Potassium ◽  
Group Ii

Abstract. Six Holstein bulls were housed in a climate-chamber under constant light regimen and after two weeks of preconditioning at 15°C, 60% relative humidity RH (day) and 12°C, 60% RH (night) were subjected to two weeks of heat exposure. This involved one week at 30°C and 60% RH (day) and 25°C and 60% RH (night) and a further week at 35°C, 60% RH (day) and 30°C, 60% RH (night). Three bulls were untreated (group I) and 3 bulls were treated (group II) just before and during heat exposure with a prolactin inhibitor to study the possible physiological role of prolactin on the regulation of water, potassium and sodium. Serum prolactin levels increased significantly (P < 0.01) in group I from the control value of 6 ng/ml to 33 and 44 ng/ml when the ambient temperature was increased (weeks 3 and 4) and then decreased to 21 and 12 ng/ml after reduction in temperature during weeks 5 and 6, respectively. For group II prolactin values decreased under the treatment with the prolactin inhibitor to 0.5 ng/ml and remained at this level throughout the experiment. GH levels were unaffected by heat treatment or by treatment with prolactin inhibitor. There were no differences between groups I and II in respiratory rate, pulse rate and rectal temperature. Water intake increased in both groups under heat exposure but decreased significantly afterwards only in group II. Differences in urinary excretion volume and blood serum osmolality were not significant. Urinary potassium and sodium excretion were unchanged in group II but increased with heat exposure in group I. During heat exposure 2 bulls of group II lost weight despite maintaining food intake.

The Protective Effect of Metformin against Oxandrolone-Induced Infertility in Male Rats

2020 ◽  
Vol 26 ◽  
Author(s):  
Abdulqader Fadhil Abed ◽  
Yazun Bashir Jarrar ◽  
Hamzeh J Al-Ameer ◽  
Wajdy Al-Awaida ◽  
Su-Jun Lee
Keyword(s):  
Gene Expression ◽  
Male Infertility ◽  
Protective Effect ◽  
Histological Examination ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Male Rats ◽  
P Value ◽  
Protective Effects ◽  
Rt Pcr

Background: Oxandrolone is a synthetic testosterone analogue that is widely used among bodybuilders and athletes. However, oxandrolone causes male infertility. Recently, it was found that metformin reduces the risk of infertility associated with diabetes mellitus. Aim: This study aimed to investigate the protective effects of metformin against oxandrolone-induced infertility in male rats. Methods: Rats continuously received one of four treatments (n=7) over 14 days: control DMSO administration, oxandrolone administration, metformin administration, or co-administration of oxandrolone and metformin. Doses were equivalent to those used for human treatment. Subsequently, testicular and blood samples were collected for morphological, biochemical, and histological examination. In addition, gene expression of the testosterone synthesizing enzyme CYP11A1 was analyzed in the testes using RT-PCR. Results: Oxandrolone administration induced male infertility by significantly reducing relative weights of testes by 48%, sperm count by 82%, and serum testosterone levels by 96% (ANOVA, P value < 0.05). In addition, histological examination determined that oxandrolone caused spermatogenic arrest which was associated with 2-fold downregulation of testicular CYP11A1 gene expression. However, co-administration of metformin with oxandrolone significantly ameliorated toxicological alterations induced by oxandrolone exposure (ANOVA, P value < 0.05). Conclusion: Metformin administration protected against oxandrolone-induced infertility in male rats. Further clinical studies are needed to confirm the protective effect of metformin against oxandrolone-induced infertility among athletes.

scholarly journals Arsenic nano complex induced degradation of YAP sensitized ESCC cancer cells to radiation and chemotherapy

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Wei Zhou ◽  
Meiyue Liu ◽  
Xia Li ◽  
Peng Zhang ◽  
Jiong Li ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Radiation Therapy ◽  
Cancer Cells ◽  
Solid Tumors ◽  
Xenograft Model ◽  
Ros Production ◽  
Protective Effects ◽  
Migration Ability ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Increased reactive oxygen species (ROS) production by arsenic treatment in solid tumors showed to be effective to sensitize cancer cells to chemotherapies. Arsenic nano compounds are known to increase the ROS production in solid tumors. Methods In this study we developed arsenic–ferrosoferric oxide conjugated Nano Complex (As2S2–Fe3O4, AFCNC) to further promote the ROS induction ability of arsenic reagent in solid tumors. We screen for the molecular pathways that are affect by arsenic treatment in ESCC cancer cells. And explored the underlying molecular mechanism for the arsenic mediated degradations of the key transcription factor we identified in the gene microarray screen. Mouse xenograft model were used to further verify the synthetic effects of AFCNC with chemo and radiation therapies, and the molecular target of arsenic treatment is verified with IHC analysis. Results With gene expression microarray analysis we found Hippo signaling pathway is specifically affected by arsenic treatment, and induced ubiquitination mediated degradation of YAP in KYSE-450 esophageal squamous cell carcinoma (ESCC) cells. Mechanistically we proved PML physically interacted with YAP, and arsenic induced degradation PML mediated the degradation of YAP in ESCC cells. As a cancer stem cell related transcription factor, YAP 5SA over expressions in cancer cells are correlated with resistance to chemo and radiation therapies. We found AFCNC treatment inhibited the increased invasion and migration ability of YAP 5SA overexpressing KYSE-450 cells. AFCNC treatment also effectively reversed protective effects of YAP 5SA overexpression against cisplatin induced apoptosis in KYSE-450 cells. Lastly, with ESCC mouse xenograft model we found AFCNC combined with cisplatin treatment or radiation therapy significantly reduced the tumor volumes in vivo in the xenograft ESCC tumors. Conclusions Together, these findings suggested besides ROS, YAP is a potential target for arsenic based therapy in ESCC, which should play an important role in the synthetic effects of arsenic nano complex with chemo and radiation therapy.

scholarly journals Protective Effects of Taurine Chloramine on Experimentally Induced Colitis: NFκB, STAT3, and Nrf2 as Potential Targets

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 479
Author(s):  
Seong Hoon Kim ◽  
Hye-Won Yum ◽  
Seung Hyeon Kim ◽  
Wonki Kim ◽  
Su-Jung Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Parent Compound ◽  
Oxidative Stress Marker ◽  
Heme Oxygenase 1 ◽  
Trinitrobenzene Sulfonic Acid ◽  
Protective Effects ◽  
Taurine Chloramine ◽  
Proinflammatory Mediators ◽  
Experimentally Induced

Taurine chloramine (TauCl) is an endogenous anti-inflammatory substance which is derived from taurine, a semi-essential sulfur-containing β-amino acid found in some foods including meat, fish, eggs and milk. In general, TauCl as well as its parent compound taurine downregulates production of tissue-damaging proinflammatory mediators, such as chemokines and cytokines in many different types of cells. In the present study, we investigated the protective effects of TauCl on experimentally induced colon inflammation. Oral administration of TauCl protected against mouse colitis caused by 2,4,6-trinitrobenzene sulfonic acid (TNBS). TauCl administration attenuated apoptosis in the colonic mucosa of TNBS-treated mice. This was accompanied by reduced expression of an oxidative stress marker, 4-hydroxy-2-nonenal and proinflammatory molecules including tumor necrosis factor-α, interleukin-6 and cyclooxygenase-2 in mouse colon. TauCl also inhibited activation of NFκB and STAT3, two key transcription factors mediating proinflammatory signaling. Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Taken together, these results suggest that TauCl exerts the protective effect against colitis through upregulation of Nrf2-dependent cytoprotective gene expression while blocking the proinflammatory signaling mediated by NFκB and STAT3.

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