PARALLEL STUDIES OF COMPLEMENT AND BLOOD COAGULATION IX. THE EFFECT OF METHIONINE, CHOLINE, AND CYSTINE ON THE CHANGES INDUCED BY ETHIONINE

1953 ◽  
Vol 31 (4) ◽  
pp. 343-357
Author(s):  
Christine E. Rice ◽  
Paul Boulanger ◽  
P. J. G. Plummer ◽  
E. Annau

Fatty livers were produced in guinea pigs by the repeated feeding or injection of ethionine; the acinar cells of the pancreas were also affected in some of the animals. Marked changes in plasma coagulability always occurred as well as a definite reduction in complement titer in which two or more of the major complement components were involved. Methionine displayed some protective effect against the fatty liver induced by the ethionine and was partially effective in controlling the coagulative changes and the decline in complement titer. In some animals, choline likewise ameliorated these conditions, whereas cystine tended to aggravate them. A combination of cystine and choline was more effective than choline alone.

1953 ◽  
Vol 31 (3) ◽  
pp. 162-172
Author(s):  
Christine E. Rice ◽  
Paul Boulanger ◽  
P. J. G. Plummer

A marked prolongation of the two-stage clotting time of the plasma was produced in guinea pigs by the repeated injection of small weekly doses of carbon tetrachloride. Ac-globulin (labile factor), as well as fibrinogen and prothrombin, was reduced. A significant fall in whole complement titer also occurred; of the four major complement components, C′ 2 and C′ 3 were the most affected. Subsequent and concurrent daily feedings of choline chloride or methionine reduced the clotting time of the plasma of certain of the carbon tetrachloride treated animals but not to normal levels; they had no significant influence on complement titer. Previous and concurrent daily feedings of choline chloride ameliorated the fatty liver condition and gave some protection against the decrease in the coagulability of the blood induced by the drug; the decline in complement titer was not prevented. Ethionine augmented the changes induced by carbon tetrachloride.


2016 ◽  
Vol 45 (4) ◽  
pp. 467-473
Author(s):  
Juyeon Kim ◽  
Yunjung Seo ◽  
Joong-Hyeop Park ◽  
Sang Kyu Noh

Toxicology ◽  
2010 ◽  
Vol 273 (1-3) ◽  
pp. 60 ◽  
Author(s):  
Hong-Yan Yu ◽  
Bao-Lian Wang ◽  
Jing Zhao ◽  
Xiao-Min Yao ◽  
Yu Gu ◽  
...  

2015 ◽  
Vol 29 (11) ◽  
pp. 1761-1767 ◽  
Author(s):  
Rana Keyhanmanesh ◽  
Saeideh Saadat ◽  
Mostafa Mohammadi ◽  
Amir-Ali Shahbazfar ◽  
Maryam Fallahi

2021 ◽  
Vol 12 ◽  
Author(s):  
Ruiwen Wang ◽  
Zhecheng Wang ◽  
Ruimin Sun ◽  
Rong Fu ◽  
Yu Sun ◽  
...  

Fatty acid β-oxidation is an essential pathogenic mechanism in nonalcoholic fatty liver disease (NAFLD), and TATA-box binding protein associated factor 9 (TAF9) has been reported to be involved in the regulation of fatty acid β-oxidation. However, the function of TAF9 in NAFLD, as well as the mechanism by which TAF9 is regulated, remains unclear. In this study, we aimed to investigate the signaling mechanism underlying the involvement of TAF9 in NAFLD and the protective effect of the natural phenolic compound Danshensu (DSS) against NAFLD via the HDAC1/TAF9 pathway. An in vivo model of high-fat diet (HFD)-induced NAFLD and a palmitic acid (PA)-treated AML-12 cell model were developed. Pharmacological treatment with DSS significantly increased fatty acid β-oxidation and reduced lipid droplet (LD) accumulation in NAFLD. TAF9 overexpression had the same effects on these processes both in vivo and in vitro. Interestingly, the protective effect of DSS was markedly blocked by TAF9 knockdown. Mechanistically, TAF9 was shown to be deacetylated by HDAC1, which regulates the capacity of TAF9 to mediate fatty acid β-oxidation and LD accumulation during NAFLD. In conclusion, TAF9 is a key regulator in the treatment of NAFLD that acts by increasing fatty acid β-oxidation and reducing LD accumulation, and DSS confers protection against NAFLD through the HDAC1/TAF9 pathway.


1995 ◽  
Vol 98 (5) ◽  
pp. 761-769,925
Author(s):  
MOTOAKI ISHIGAKI ◽  
KATSUHISA IKEDA ◽  
HIROSHI SUNOSE ◽  
MASAAKI SUZUKI ◽  
TOMONORI TAKASAKA
Keyword(s):  

Drug Research ◽  
2018 ◽  
Vol 68 (10) ◽  
pp. 553-559
Author(s):  
Golbahar Saeedi ◽  
Fereshteh Jeivad ◽  
Mohammadhadi Goharbari ◽  
Gholamreza Gheshlaghi ◽  
Omid Sabzevari

Abstract Background Non-alcoholic fatty liver (NAFLD) is one the most prevalent disease worldwide which characterized by fat accumulation in liver with no established efficient therapy. We designed this study to investigate protective and therapeutic effect of Crataegus oxyacantha L. (C. oxyacantha) on NAFLD induced by high fat diet in rat models. Methods NAFLD was induced by High Fat Diet+fructose (HFD), 45 Wistar rats were divided to 8 groups including control, HFD, HFD+diet change, HFD+diet change+C. oxyacantha 20 mg/kg, co treatment of HFD+C. oxyacantha 10, 20 and 40 mg/kg, and normal diet+C. oxyacantha 40 mg. C. oxyacantha was administered orally. Effectiveness of the C. oxyacantha was assessed through measuring the biochemical factors, and oxidative stress marker (FRAP, GSH, and MDA). Histopathological study was performed using H & E staining. Results The diet change from high fat to low fat ameliorated liver damage. However, consumption of C. oxyacantha (10 & 20 mg/kg) caused significant reduction in the level of all examined liver biomarkers specially LDH, that showed C. oxyacantha can restore the hepatocyte damage due to HFD. The C. oxyacantha showed a protective effect which was more prominent in the animals treated with the 20 mg/kg C. oxyacantha. The administration of C. oxyacantha caused increased antioxidant status (GSH and FRAP levels) and decreased lipid peroxidation in treated animals. Major Conclusion Accordingly, C. oxyacantha have both therapeutic and protective effect for NAFLD and may be a potential candidate for further assessments in clinical studies.


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