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Fasting enhances biochemical and histopathological changes of isoniazid induced liver injury in mouse

By: Xu, Qin.
Contributor(s): Ren, Zhihui.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2021Edition: Vol.83(2), March-April.Description: 336-345p.Subject(s): PHARMACEUTICSOnline resources: Click here In: Indian journal of pharmaceutical sciencesSummary: Fasting can up regulate the expression of cytochrome P450 2E1 and induce glutathione levels to decrease, protecting the liver from hepatotoxic agents. The aim of this study was to research the mechanism of fasting aggravates isoniazid induced liver injury in mouse. 7 w old male C57 black 6 mice were randomly assigned to two groups: mice fed ad libitum on commercial chow (A group) and mice fasted for 12 h during the day and fed ad libitum on commercial chow (F group). All animals were administered with 100 mg/kg of isoniazid daily by gavage for 6 w (isoniazid levels were selected on basis of screening multiple concentrations). Sera were collected to measure biochemical parameters. Liver sections were stained with hematoxylin and eosin to evaluate hepatic histology. Cytokines was detected by cytometric bead array, flow cytometry. Isoniazid administration (100 mg/kg) daily for 6 w did not significantly induce histological damage in mice of A group. Compared with normal mice, there was no signi ficant difference in serum alanine aminotransferase and aspartate aminotransferase. However, the level of alanine aminotransferase and aspartate aminotransferase levels in F group remained elevated for 6 w, reached its peak on the 3 rd d and gradually returned to normal. The liver sections revealed hepatic edema around the central vein on the 3rd d. At 1st or 2nd w, hepatic edema around the central vein with in flammatory cell infiltration and focal necrosis was present. After 4 w, liver histology gradually recovered. Fasting condition in fluences the cytokine concentration in peripheral blood and liver tissue.
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Fasting can up regulate the expression of cytochrome P450 2E1 and induce glutathione levels to decrease,
protecting the liver from hepatotoxic agents. The aim of this study was to research the mechanism of
fasting aggravates isoniazid induced liver injury in mouse. 7 w old male C57 black 6 mice were randomly
assigned to two groups: mice fed ad libitum on commercial chow (A group) and mice fasted for 12 h
during the day and fed ad libitum on commercial chow (F group). All animals were administered with 100
mg/kg of isoniazid daily by gavage for 6 w (isoniazid levels were selected on basis of screening multiple
concentrations). Sera were collected to measure biochemical parameters. Liver sections were stained with
hematoxylin and eosin to evaluate hepatic histology. Cytokines was detected by cytometric bead array,
flow cytometry. Isoniazid administration (100 mg/kg) daily for 6 w did not significantly induce histological
damage in mice of A group. Compared with normal mice, there was no signi ficant difference in serum
alanine aminotransferase and aspartate aminotransferase. However, the level of alanine aminotransferase
and aspartate aminotransferase levels in F group remained elevated for 6 w, reached its peak on the 3 rd
d and gradually returned to normal. The liver sections revealed hepatic edema around the central vein
on the 3rd d. At 1st or 2nd w, hepatic edema around the central vein with in flammatory cell infiltration and
focal necrosis was present. After 4 w, liver histology gradually recovered. Fasting condition in fluences the
cytokine concentration in peripheral blood and liver tissue.

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