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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Tournefortia sarmentosa extract attenuates acetaminophen-induced hepatotoxicity.
Pharmaceutical Biology 2012 March
CONTEXT: Tournefortia sarmentosa Lam. (Boraginaceae), a Chinese herbal medicine, is commonly used as a detoxicant or anti-inflammatory agent.
OBJECTIVE: As acetaminophen (APAP) is a well-known hepatotoxin, we investigated the effect of the aqueous extract of the T. sarmentosa on APAP-induced hepatotoxicity in vivo and in vitro.
MATERIALS AND METHODS: Levels of liver function markers serum glutamate oxaloacetate transaminase (SGOT), glutamate pyruvate transaminase (SGPT), and alkaline phosphatase (ALP), inflammatory markers tumor necrosis factor (TNF)-α, interleukin (IL)-1b, and IL-6 in serum, and antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), as well as lipid peroxidation were determined.
RESULTS: T. sarmentosa significantly reduced the elevated liver function (SGOT, SGPT, and ALP, p < 0.01) and inflammatory markers (TNF-α, IL-1β, and IL-6, p < 0.01) in serum of APAP-intoxicated rats. Malondialdehyde level (p < 0.05) and antioxidant enzyme levels (CAT, SOD, and GPx, p < 0.05) were also reduced in APAP-intoxicated rats treated with T. sarmentosa. Incubation of rat hepatocyte cell line clone-9 cells with APAP reduced cell viability and increased the extent of lipid peroxidation. APAP stimulation also reduced the level of glutathione (GSH) and caused reduction in the activities of the antioxidant enzymes, CAT, SOD, and GPx. Pretreatment of hepatocytes with T. sarmentosa aqueous extract before and during APAP stimulation attenuated the extent of lipid peroxidation, increased cell viability and GSH level, and enhanced the activities of antioxidant enzymes.
DISCUSSION AND CONCLUSION: These data suggest that the aqueous extract of T. sarmentosa can prevent APAP-induced hepatotoxicity.
OBJECTIVE: As acetaminophen (APAP) is a well-known hepatotoxin, we investigated the effect of the aqueous extract of the T. sarmentosa on APAP-induced hepatotoxicity in vivo and in vitro.
MATERIALS AND METHODS: Levels of liver function markers serum glutamate oxaloacetate transaminase (SGOT), glutamate pyruvate transaminase (SGPT), and alkaline phosphatase (ALP), inflammatory markers tumor necrosis factor (TNF)-α, interleukin (IL)-1b, and IL-6 in serum, and antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), as well as lipid peroxidation were determined.
RESULTS: T. sarmentosa significantly reduced the elevated liver function (SGOT, SGPT, and ALP, p < 0.01) and inflammatory markers (TNF-α, IL-1β, and IL-6, p < 0.01) in serum of APAP-intoxicated rats. Malondialdehyde level (p < 0.05) and antioxidant enzyme levels (CAT, SOD, and GPx, p < 0.05) were also reduced in APAP-intoxicated rats treated with T. sarmentosa. Incubation of rat hepatocyte cell line clone-9 cells with APAP reduced cell viability and increased the extent of lipid peroxidation. APAP stimulation also reduced the level of glutathione (GSH) and caused reduction in the activities of the antioxidant enzymes, CAT, SOD, and GPx. Pretreatment of hepatocytes with T. sarmentosa aqueous extract before and during APAP stimulation attenuated the extent of lipid peroxidation, increased cell viability and GSH level, and enhanced the activities of antioxidant enzymes.
DISCUSSION AND CONCLUSION: These data suggest that the aqueous extract of T. sarmentosa can prevent APAP-induced hepatotoxicity.
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