Effect of malotilate (diisopropyl 1,3-dithiol-2-ylidenemalonate) on the protein synthesis in rat liver.

Imaizumi, Yohko; Katoh, Minoru; Sugimoto, Tatsuyoshi; Kasai, Tamotsu

doi:10.1254/jjp.32.369

Cited by 22 publications

(3 citation statements)

References 16 publications

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“…The treatment of c-SST-2 cells with MT did not modify their metastasis-associated properties, such as adhesion and invasion into the RLE cell monolayer or basement membrane, gelatinase production and migration activity in vitro [17]. On the other hand, in vitro invasion of the RLE monolayer by c-SST- Regarding the pharmacological action of MT, it has been revealed that MT stimulates RNA and protein synthesis and glucose metabolism in the liver and cultured hepatocytes [12][13][14] and that MT modulates the functions of various types of cells other than hepatocytes [11,15]. Sunada et al [16] reported that MT developed the cobblestone-shaped cell monolayer on bovine endothelial cells in longterm culture and promoted the formation of adherence junctions.…”

Section: Discussionmentioning

confidence: 93%

Inhibitory Effects of Malotilate on in vitro Invasion of Lung Endothelial Cell Monolayer by Human Oral Squamous Cell Carcinoma Cells

Shibata¹,

Nagayasu²,

Hamada³

et al. 2000

Tumor Biology

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We have previously reported that malotilate (MT) inhibited the invasion and metastasis of rat mammary carcinoma cells through the modification of host endothelial cells. In this study, we examined the inhibitory effects of MT on invasion of human cancer, using five oral squamous cell carcinoma cells (SAS, Ca9-22 and HSC-2, -3 and -4). MT did not affect the growth of these tumor cells and the invasion of reconstituted basement membrane, Matrigel. In an in vitro invasion assay using rat lung endothelial (RLE) cells, invasion of tumor cells which had been treated with MT (10 ng/ml, 24 h) was not affected; however, when RLE cells had been treated with MT, invasion was significantly inhibited in three cell lines (SAS, Ca9-22 and HSC-4) and a tendency to inhibition was also observed in other cell lines. Electron-microscopical examination of the RLE monolayer treated with MT (MT-RLE) showed the development of gap and tight junction-like structures. Subsequently, junction-associated proteins, connexin 43, zonula occludin and desmoglein, were examined by Western blotting. Protein levels of connexin 43 and zonula occludin were elevated dose dependently, and connexin 43 was chronologically enhanced by MT whereas desmoglein was not. The enhanced gap junctional communication of MT-RLE cells was observed in the scrape-loading assay using lucifer yellow CH. These results suggest that MT promotes the development of cell-to-cell adhesion, e.g. gap junction and tight junction in endothelial cells, resulting in the inhibition of invasion by the tumor cells.

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Section: Discussionmentioning

confidence: 93%

Inhibitory Effects of Malotilate on in vitro Invasion of Lung Endothelial Cell Monolayer by Human Oral Squamous Cell Carcinoma Cells

Shibata¹,

Nagayasu²,

Hamada³

et al. 2000

Tumor Biology

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“…These observations confirm the restorative effect of malotilate on ethanol induced hepatic damage. Imaizumi and Kato (1981) 12 and Niwano and Katoh (1985) 13 reported restorative effect of malotilate on the liver as increase in liver weight and liver protein attributed to increase in RNA and DNA contents in the liver. Similar findings have been reported by Igarashi, Hatahara and Funaki (1983) that malotilate offers hepatotrophic action by increase in protein synthesis in hepatectomised rats 14 .…”

Section: Graph 1: Effect Of Malotilate (Day 22to 42) On Ethanol (Day mentioning

confidence: 99%

Untitled

2016

IJPSR

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Background: In chronic alcoholics, continuous heavy drinking leads to progression of alcoholic liver disease (ALD) from alcoholic fatty liver, hepatitis to cirrhosis. Strict abstinence from alcohol has its own limitations and there is paucity of promising drugs available to treat ALD. Malotilate showed promising hepatocyte regenerating capacity and ability to prevent such damage. Aims: The objective of this study was to evaluate curative effect of malotilate on ALD in rats. Methods: The study was done using Sprague Dawley rats. 5 groups were treated as: 1. Control: ethanol 40% v/v (orally 1ml / 100 g / d), 2. Vehicle control: Methyl Cellulose and 3, 4, 5: malotilate, three doses 25 (Low), 50 (Moderate), 100 (High) mg /kg / d orally, respectively. In all groups: ethanol was given initially for 21 days. Then vehicle or malotilate was administered for next 21 days. The liver damage was assessed biochemically on day-1, day-22, day-43 by measuring serum AST, ALT, ALP, GGT, total bilirubin, direct bilirubin, total protein, albumin and prothrombin time. The histo-pathological assessment of liver damage was done on day-43. Results: This study demonstrated that malotilate favorably altered all the biochemical parameters and the histopathology scores of liver damage in malotilate treated groups. Conclusions: malotilate showed hepatic structure regenerative and hepatic function restorative effect in ALD. This study indicated that malotilate may be useful in treating established ALD in alcoholics.

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“…A repeated dose of 1,000 mg/kg caused a 20-30% decrease Malotilate (diisopropyl 1,3-dithiol-2 ylidenemalonate) has a hepatotropic effect, in particular improving protein metabolism in the liver (1). It causes marked improvements in reduced serum cholesterol and albumin levels and improves cholinesterase activity both in rats with carbon tetrachloride induced liver damage and in patients with chronic hepatitis and liver cirrhosis.…”

Section: Effects Of Malotilate On Rat Erythrocytesmentioning

confidence: 99%