scholarly journals Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats

1999 ◽  
Vol 276 (3) ◽  
pp. G622-G628 ◽  
Author(s):  
Shiro Yokohama ◽  
Masashi Yoneda ◽  
Kimihide Nakamura ◽  
Isao Makino
Keyword(s):  
Nervous System ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Sympathetic Nerves ◽  
Bile Secretion ◽  
Corticotropin Releasing Factor ◽  
Intracisternal Injection ◽  
6 Hydroxydopamine ◽  
The Brain

Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of intracisternal CRF on carbon tetrachloride (CCl4)-induced acute liver injury was examined in rats. Intracisternal injection of CRF dose dependently enhanced elevation of the serum alanine aminotransferase (ALT) level induced by CCl4. Elevations of serum aspartate aminotransferase, alkaline phosphatase, and total bilirubin levels by CCl4were also enhanced by intracisternal CRF injection. Intracisternal injection of CRF also aggravated CCl4-induced hepatic histological changes. Intracisternal CRF injection alone did not modify the serum ALT level. Intravenous administration of CRF did not influence CCl4-induced acute liver injury. The aggravating effect of central CRF on CCl4-induced acute liver injury was abolished by denervation of hepatic plexus with phenol and by denervation of noradrenergic fibers with 6-hydroxydopamine treatment but not by hepatic branch vagotomy or atropine treatment. These results suggest that CRF acts in the brain to exacerbate acute liver injury through the sympathetic-noradrenergic pathways.

Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats

2002 ◽  
Vol 282 (6) ◽  
pp. R1782-R1788 ◽  
Author(s):  
Yukiomi Nakade ◽  
Masashi Yoneda ◽  
Kimihide Nakamura ◽  
Isao Makino ◽  
Akira Terano
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Receptor Antagonist ◽  
Acute Liver Injury ◽  
Bile Secretion ◽  
Liver Sample ◽  
Histological Changes ◽  
6 Hydroxydopamine ◽  
The Brain

Central neuropeptides play important roles in many physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Central injection of corticotropin-releasing factor (CRF) aggravates carbon tetrachloride (CCl4)-induced acute liver injury through the sympathetic nervous pathway in rats. However, still nothing is known about a role of endogenous neuropeptides in the brain in hepatic pathophysiological regulations. Involvement of endogenous CRF in the brain in CCl4-induced acute liver injury was investigated by centrally injecting a CRF receptor antagonist in rats. Male fasted Wistar rats were injected with CRF receptor antagonist α-helical CRF-(9–41) (0.125–5 μg) intracisternally just before and 6 h after CCl4 (2 ml/kg) administration, and blood samples were obtained before and 24 h after CCl4 injection for measurement of hepatic enzymes. The liver sample was removed 24 h after CCl4 injection, and histological changes were examined. Intracisternal α-helical CRF-(9–41) dose dependently (0.25–2 μg) reduced the elevation of alanine aminotransferase and aspartate aminotransferase levels induced by CCl4. Intracisternal α-helical CRF-(9–41) reduced CCl4-induced liver histological changes, such as centrilobular necrosis. The effect of central CRF receptor antagonist on CCl4-induced liver injury was abolished by sympathectomy and 6-hydroxydopamine pretreatment but not by hepatic branch vagotomy or atropine pretreatment. These findings suggest the regulatory role of endogenous CRF in the brain in experimental liver injury in rats.

Central injection of a novel corticotropin-releasing factor(CRF)antagonist, astressin, protects carbon tetrachloride (CC14)-induced acute liver injury in rats

2000 ◽  
Vol 118 (4) ◽  
pp. A430
Author(s):  
Yukiomi Nakade ◽  
Masashi Yoneda ◽  
Shuujirou Takamoto ◽  
Shirou Yokohama ◽  
Mitsuyoshi Okada ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Corticotropin Releasing Factor

Central nervous system action of corticotropin-releasing factor to inhibit gastric emptying in rats

1987 ◽  
Vol 253 (2) ◽  
pp. G241-G245 ◽  
Author(s):  
Y. Tache ◽  
M. Maeda-Hagiwara ◽  
C. M. Turkelson
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gastric Emptying ◽  
Corticotropin Releasing Factor ◽  
Phenol Red ◽  
Liquid Meal ◽  
Intracisternal Injection ◽  
The Central Nervous System ◽  
Long Acting ◽  
The Brain

The present study evaluates the central nervous system action of rat corticotropin-releasing factor (CRF) on gastric emptying of a liquid meal in conscious rats using the phenol red method. Intracisternal injection of CRF (63-210 pmol) dose-dependently inhibited gastric emptying of a liquid meal by 37-80%. Peptide action was rapid in onset, long acting, and not mimicked by intracisternal injection of growth hormone-releasing factor. Intracisternal CRF-induced inhibition of gastric emptying was reversed by subdiaphragmatic vagotomy but not by naloxone pretreatment or adrenalectomy. Intravenous injection of CRF (21-630 pmol) also dose-dependently inhibited gastric emptying. CRF antiserum blocked the effect of intravenous but not of intracisternal injection of CRF (63 pmol). These results demonstrated that CRF injected in a picomole amount into the cerebrospinal fluid acts within the brain to inhibit gastric emptying of a liquid meal through vagal-dependent pathways.

Restraint stress exacerbates carbon tetrachloride-induced liver injury in rats: A role of endogenous corticotropin-releasing factor (CRF) in the brain

2001 ◽  
Vol 120 (5) ◽  
pp. A715
Author(s):  
Yukiomi Nakade ◽  
Masashi Yoneda ◽  
Shujiro Takamoto ◽  
Taku Ito ◽  
Satoshi Okamoto ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Restraint Stress ◽  
Corticotropin Releasing Factor ◽  
The Brain

Aloe-Emodin Quinone Pretreatment Reduces Acute Liver Injury Induced by Carbon Tetrachloride

2000 ◽  
Vol 87 (5) ◽  
pp. 229-233 ◽  
Author(s):  
Beatrice Arosio ◽  
Nicoletta Gagliano ◽  
Lorena Maria Pia Fusaro ◽  
Luciano Parmeggiani ◽  
Jacopo Tagliabue ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Aloe Emodin

Explore the mechanism of Swertia mussotii Franch. for hepatoprotective effects with iTRAQ-LC-MS/MS

2020 ◽  
Vol 23 ◽  
Author(s):  
Haixia Yun ◽  
Xinyu Wu ◽  
Yiwei Ding ◽  
Wendou Xiong ◽  
Xianglan Duan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Aspartate Aminotransferase ◽  
Alanine Aminotransferase ◽  
Total Bilirubin ◽  
Acute Liver Injury ◽  
Proteome Analysis ◽  
Ppi Networks ◽  
Hepatoprotective Effects

Background and Objective : A Tibetan traditional herb named Swertia mussotii Franch., also called “Zangyinchen” by the local people of Qinghai-Tibet area, has been used to protect the liver from injury for many years. However, the curative effect and molecular mechanism of the herb have not been demonstrated clearly. Materials and Methods: In our study, serum alanine aminotransferase, aspartate aminotransferase, total bilirubin levels were examined after S. mussotii Franch. treatment in the acute liver injury of the carbon tetrachloride-induced rat model. Then, Proteome Analysis was applied to explore the potential mechanism of SMT for hepatoprotective effects after iTRAQLC-MS/MS analysis (isobaric tag for relative and absolute quantification-liquid chromatograph-mass spectrometer with tandem mass spectrometry). Results: Serum results showed, alanine aminotransferase, aspartate aminotransferase, total bilirubin levels of rats with acute liver injury were all improved with SMT treatment. Moreover, Proteome Analysis suggested that, with S. Mussotii Franch. treatment, the levels of lipid catabolic process and lipid homeostasis were all enhanced. And the results of protein-protein interaction (PPI) analysis illustrated that these proteins assembled in PPI networks were found almost significantly enriched in response to lipid, negative regulation of lipase activity, response to lipopolysaccharide etc. Furthermore, the downregulated MRP14 and MRP8 proteins were found involved in the lipid metabolism, which may indicate the mechanism of SMT protection liver from ALI induced by carbon tetrachloride. Conclusion: SMT herb could play a role in hepatoprotection and alleviate the effect of acute liver injury by impacting the lipid metabolism associated biological process.

scholarly journals Lemon Balm and Dandelion Leaf Extracts Synergistically Protect against Carbon Tetrachloride-Induced Acute Liver Injury in Mice

2021 ◽  
Vol 11 (1) ◽  
pp. 390
Author(s):  
Beom-Rak Choi ◽  
Il-Je Cho ◽  
Su-Jin Jung ◽  
Jae-Kwang Kim ◽  
Dae-Geon Lee ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Antioxidant Activities ◽  
Body Weight Gain ◽  
Histopathological Analysis ◽  
Related Factor ◽  
Mrna Levels ◽  
Protective Effects ◽  
Lemon Balm

Lemon balm and dandelion are commonly used medicinal herbs exhibiting numerous pharmacological activities that are beneficial for human health. In this study, we explored the protective effects of a 2:1 (w/w) mixture of lemon balm and dandelion extracts (MLD) on carbon tetrachloride (CCl4)-induced acute liver injury in mice. CCl4 (0.5 mL/kg; i.p.) injection inhibited body weight gain and increased relative liver weight. Pre-administration of MLD (50–200 mg/kg) for 7 days prevented these CCl4-mediated changes. In addition, histopathological analysis revealed that MLD synergistically alleviated CCl4-mediated hepatocyte degeneration and infiltration of inflammatory cells. MLD decreased serum aspartate aminotransferase and alanine transferase activities and reduced the number of liver cells that stained positive for cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase, suggesting that MLD protects against CCl4-induced hepatic damage via the inhibition of apoptosis. Moreover, MLD attenuated CCl4-mediated lipid peroxidation and protein nitrosylation by restoring impaired hepatic nuclear factor erythroid 2-related factor 2 mRNA levels and its dependent antioxidant activities. Furthermore, MLD synergistically decreased mRNA and protein levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the liver. Together, these results suggest that MLD has potential for preventing acute liver injury by inhibiting apoptosis, oxidative stress, and inflammation.

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