scholarly journals Regulation of bacterial lipopolysaccharide in liver toxicity caused by chlorpromazine and Z24 in Sprague-Dawley rats

2015 ◽  
Vol 4 (2) ◽  
pp. 432-441
Author(s):  
Wu Chun-qi ◽  
Li Yu-feng ◽  
Zheng Zhi-bing ◽  
Dong Yan-sheng ◽  
Yuan Ben-li ◽  
...  

LPS-induced inflammatory response could be used to establish screening models for ILT and provides a new way to reduce liver toxicity of Z24.

1997 ◽  
Vol 3 (S2) ◽  
pp. 51-52
Author(s):  
B.J. Cornell ◽  
A. Singh ◽  
I. Chu

Polyhalogenated aromatic compounds such as polychlorinated biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins (PCDDs) continue to be environmental contaminants because of their bioaccumulation in the food chain and high resistance to biodegradation. The current study was undertaken to determine if a mixture of PCB congeners (WHO-IPCS) were interactive with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in producing morphological changes in the rat liver. Both compounds are known to produce a broad range of biochemical and morphological alterations including enzyme induction.Groups (N=5) of female Sprague-Dawley rats were administered TCDD (0, 2.5, 25, 250, 1000 ng/kg bw/day) or PCB (0, 2, 20 μg/kg bw/day) alone, or in combination with each concentration of both compounds. Incorrect concentrations were published in a previous abstract. The test substance was mixed with corn oil and given by gavage at 2 ml/kg daily for 28 days. At the end of the experiment, the rats were killed and liver samples were prepared for transmission electron microscopy.


Toxins ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 398 ◽  
Author(s):  
Tarana Arman ◽  
Katherine D. Lynch ◽  
Michelle L. Montonye ◽  
Michael Goedken ◽  
John D. Clarke

Microcystin-LR (MCLR) is a hepatotoxic cyanotoxin reported to cause a phenotype similar to nonalcoholic steatohepatitis (NASH). NASH is a common progressive liver disease that advances in severity due to exogenous stressors such as poor diet and toxicant exposure. Our objective was to determine how sub-chronic MCLR toxicity affects preexisting diet-induced NASH. Sprague-Dawley rats were fed one of three diets for 10 weeks: control, methionine and choline deficient (MCD), or high fat/high cholesterol (HFHC). After six weeks of diet, animals received vehicle, 10 µg/kg, or 30 µg/kg MCLR via intraperitoneal injection every other day for the final 4 weeks. Incidence and severity scoring of histopathology endpoints suggested that MCLR toxicity drove NASH to a less fatty and more fibrotic state. In general, expression of genes involved in de novo lipogenesis and fatty acid esterification were altered in favor of decreased steatosis. The higher MCLR dose increased expression of genes involved in fibrosis and inflammation in the control and HFHC groups. These data suggest MCLR toxicity in the context of preexisting NASH may drive the liver to a more severe phenotype that resembles burnt-out NASH.


2020 ◽  
Author(s):  
Stephen Antwi ◽  
Daniel Oduro-Mensah ◽  
David Darko Obiri ◽  
Clara Lewis ◽  
Ebenezer Oduro-Mensah ◽  
...  

Abstract Ethnopharmacological relevance In Ghanaian folk medicine, Holarrhena floribunda has anecdotal use for the treatment of inflammatory conditions. A hydro ethanol extract of the stem bark has previously been shown to be effective in the management of acute inflammation and anaphylaxis in rodents.Aim of the study This study was aimed at evaluating the usefulness of H. floribunda stem bark hydro ethanol extract (HFE) for the management of chronic inflammation in a murine model.Materials and Methods Anti-arthritic effect of the extract was evaluated using Complete Freund’s Adjuvant-induced arthritis in male Sprague-Dawley rats. Using both prophylactic and therapeutic treatment models, parameters assessed included oedema, serology of inflammatory response, radiology, bone tissue histology and haematology. Data were analysed by ANOVA followed by Tukey’s multiple comparisons post hoc test.Results HFE at 50–500 mg/kg dose-dependently [P ≥ 0.0354 (prophylactic) and P ≥ 0.0001 (therapeutic)] inhibited swelling of the injected paw upon prophylactic [≤ 81.26 % (P < 0.0001)] or therapeutic [≤ 67.92 % (P < 0.01)] administration — and prevented spread of arthritis to the contralateral paw. Inflammation alleviation activity of HFE was further demonstrated by decrease in arthritis score, radiologic score and erythrocyte sedimentation rate. HFE at all doses significantly reduced serum IL-1α (P < 0.0197), and 500 mg/kg HFE reduced serum IL-6 (P = 0.0032). In contrast, serum concentrations of IL-10, protein kinase A and cyclic adenosine monophosphate were enhanced (P ≤ 0.0436). HFE consistently showed better prophylactic activity than when administered therapeutically.Conclusions The data demonstrate that HFE suppresses CFA-induced arthritis and modulates regulators of inflammation; including IL-1α, -6 and -10 which also play mediatory roles in several immune response pathways. These make HFE a strong candidate for development as an agent for management and modulation of inflammation and the inflammatory response, including immune response-related adverse events such as seen in severe COVID-19.


Pharmacology ◽  
2019 ◽  
Vol 105 (9-10) ◽  
pp. 522-530 ◽  
Author(s):  
Nancy S. Younis

<b><i>Introduction:</i></b> The clinical use of doxorubicin (DOX) is challenged by its incremental dose-related cardiotoxicity. <b><i>Objective:</i></b> The aim of the hereby study was to investigate sandalwood essential oil (SEO) against DOX-induced cardiac toxicity. <b><i>Methods:</i></b> Male Sprague-Dawley rats were allocated into 4 groups. Groups 1 signified the control, whereas group 2 administered 100 mg/kg/day SEO, both act as control. In group 3, DOX was given intraperitoneal in a dose of 3 mg/kg/ every other day for 2 weeks to induced cardiotoxicity. While group 4 received a combination of SEO and DOX for 2 weeks. DOX prompted variations were assessed by measuring cardiac injury biomarkers, including creatine phosphokinase, cardiac troponin T, and lactate dehydrogenase (LDH), electrocardiogram (ECG) fluctuations, heart rate (HR), and blood pressure (BP) indices. The effect of both DOX and SEO on various antioxidants such as glutathione, superoxide dismutase, and catalase and inflammatory mediators including interleukin-1β, tumor necrosis factor-alpha, and NF-κB was quantified. <b><i>Results:</i></b> DOX augmented cardiac injury biomarkers, altered ECG, deceased HR and antioxidants, and finally increased BP indices. Treatment with SEO significantly (<i>p</i> &#x3c; 0.05) decreased cardiac biomarkers and reversing ECG changes and BP. Moreover, treatment with SEO enhanced HR anomalies and antioxidant activity reduction and precluded the intensive inflammatory response induced by DOX. <b><i>Conclusion:</i></b> SEO may have the potential of mitigating cardiac rhythm and BP indices changes induced with DOX. SEO modifications may be due to antioxidant capacity improvement and inflammatory response prohibition of the heart muscle.


Inflammation ◽  
2020 ◽  
Vol 43 (3) ◽  
pp. 937-950 ◽  
Author(s):  
Meenakshi Bhardwaj ◽  
Veeresh Kumar Sali ◽  
Sugumar Mani ◽  
Hannah R. Vasanthi

2021 ◽  
Author(s):  
Ayobami Dare ◽  
Mahendra Channa ◽  
Anand Nadar

Abstract Diabetic-induced liver toxicity is a serious complication that cause significant metabolic dysfunction. L-ergothioneine (L-egt) is a bioactive nutraceutical obtained from mushrooms and certain food products, with reported cytoprotective, antioxidant and anti-inflammatory properties and potential to improve efficacy of existing therapy. Thus, this study evaluates the effects of L-egt, and/or metformin, on diabetes-induced liver injury. Diabetes was induced in male Sprague-Dawley rats using 10% fructose for two weeks, followed by a single low dose streptozotocin (STZ, 40 mg/kg i.p) injection. After induction of diabetes, animals were treated either with de-ionized water (DW), L-egt (35 mg/kg bwt), metformin (500 mg/kg bwt), or a combination of L-egt and metformin orally for seven weeks. Body weight and glucose were monitored during the experiment. At the completion of experiment, blood samples were collected, and liver tissue was excised for biochemical analysis, enzyme-link immunosorbent assay (ELISA) of various liver function biomarkers, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis of genes associated with inflammation, oxidative stress, and lipid metabolism, as well as histopathological evaluation. Diabetic animals showed liver hypertrophy, increased liver injury, hepatic triglycerides, oxidative stress, and hepatic inflammation. However, L-egt, and/or metformin, improved glycemic control, reduced liver injury, triglycerides, oxidative damage, inflammatory injury, and normalize liver histology by upregulating Nrf2/Sirt1, downregulate NF-kB/TGF-B1, and reduce SREBP1c/FAS expression. In conclusion, these results showed that combination of L-egt and metformin improve therapeutic efficacy than either treatment alone. Thus, L-egt can be used as an adjuvant to mitigate diabetes-induced liver complication.


2021 ◽  
Vol 1 (3) ◽  
pp. 13-25
Author(s):  
Mahendra Kumar Trivedi ◽  
Alice Branton ◽  
Dahryn Trivedi ◽  
Snehasis Jana

The study was aimed to evaluate the antioxidant and anti-inflammatory activity of the Biofield Energy Treated Proprietary Test Formulation and Biofield Energy Treatment per se to the animals on Cecal Slurry, LPS and E. coli-induced systemic inflammatory response syndrome (SIRS) model in Sprague Dawley rats. In this experiment, different antioxidants biomarkers such as myeloperoxidase (MPO), superoxide dismutase (SOD), lipid peroxidase (LPO) and cytokines like interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-2 (MIP-2) were analysed using ELISA assay in brain homogenate. A test formulation was formulated including minerals (magnesium, zinc, calcium, selenium, and iron), vitamin C, B6, E, B12, D3, β-carotene, cannabidiol isolate,and Panax ginseng extract. The component of the test formulation were divided into two parts; one section was defined as the untreated, while the other portion of each constituent and three group of animals received Biofield Energy Healing/Blessing Treatment remotely for about 3 minutes by Mr. Mahendra Kumar Trivedi, a renowned spiritual Energy Healer. The level of MPO was significantly (p≤0.001) reduced by 19.43%, 34.91%, 25.43%, 25.29% and 30.33% in the G5 (Cecal Slurry, LPS and E. coli + Biofield Energy Treated test formulation); G6 (Cecal Slurry, LPS and E. coli + Biofield Energy Treatment per se to animals from day -15); G7 (Cecal Slurry, LPS and E. coli + Biofield Energy Treated test formulation from day -15); G8 (Cecal Slurry, LPS and E. coli + Biofield Energy Treatment per se + Biofield Energy Treated/Blessed test formulation from day -15), and G9 (Cecal Slurry, LPS and E. coli + Biofield Energy Treatment per se animals + untreated test formulation) groups, respectively as compared to the untreated test formulation (G4) group. Moreover, the level of SOD was significantly increased by 45.02% (p≤0.001), 16.59%, and 35.99% (p≤0.001) in the G6, G7, and G9 groups, respectively as compared to G4 group. The level of TNF-α was significantly decreased by 12.66%, 46.92% (p≤0.001), 26.57% (p≤0.001), 23.22% (p≤0.001), and 54.28% (p≤0.001) in G5, G6, G7, G8, and G9 groups, correspondingly with reference to G4 group. Moreover, the level of IL-6 was significantly (p≤0.001) decreased by 37.51%, 20.28%, 21.55%, and 33.4% in the G6, G7, G8, and G9 groups, respectively as compared to the G4 group. Additionally, the level of MIP-2 was significantly (p≤0.001) reduced by 47.97%, 17.08%, 20.16% and 26.84% in the G6, G7, G8, and G9 groups, respectively as compared to the G4 group. Together, the data imply the antioxidant and anti-inflammatory potential of the Biofield Energy Treated test formulation and Biofield Energy Treatment per se along with preventive measure on the animal with respect to various inflammatory conditions that might be beneficial various types of systemic inflammatory disorders specially sepsis, trauma, septic shock or any types of injuries. Therefore, the results described a significant reduction of inflammation-related disease progression rate and its complications in the preventive maintenance groups (viz. G6, G7, G8, and G9).


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