A novel role of alkaline phosphatase in protection from immunological liver injury in mice

2002 ◽  
Vol 22 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Qiang Xu ◽  
Zhaohua Lu ◽  
Xianming Zhang
Keyword(s):  
Alkaline Phosphatase ◽  
Liver Injury

scholarly journals Antioxidative Role of Hatikana (Leea macrophyllaRoxb.) Partially Improves the Hepatic Damage Induced by CCl4in Wistar Albino Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Samina Akhter ◽  
Md. Atiar Rahman ◽  
Jannatul Aklima ◽  
Md. Rakibul Hasan ◽  
J. M. Kamirul Hasan Chowdhury
Keyword(s):  
Alkaline Phosphatase ◽  
Liver Injury ◽  
Total Protein ◽  
Aspartate Aminotransferase ◽  
Alanine Aminotransferase ◽  
Biochemical Parameters ◽  
Lipid Profiles ◽  
Scavenging Effect ◽  
Serum Aspartate Aminotransferase

This research investigated the protective role ofLeea macrophyllaextract on CCl4-induced acute liver injury in rats. Different fractions ofLeea macrophylla(Roxb.) crude extract were subjected to analysis for antioxidative effects. Rats were randomly divided into four groups as normal control, hepatic control, and reference control (silymarin) group and treatment group. Evaluations were made for the effects of the fractions on serum enzymes and biochemical parameters of CCl4-induced albino rat. Histopathological screening was also performed to evaluate the changes of liver tissue before and after treatment. Different fractions ofLeea macrophyllashowed very potent 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging effect, FeCl3reducing effect, superoxide scavenging effect, and iron chelating effect. Carbon tetrachloride induction increased the level of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) and other biochemical parameters such as lipid profiles, total protein, and CK-MB. In contrast, treatment ofLeea macrophyllareduced the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) activities as well as biochemical parameters activities.L. macrophyllapartially restored the lipid profiles, total protein, and CK-MB. Histopathology showed the treated liver towards restoration. Results evidenced thatL. macrophyllacan be prospective source of hepatic management in liver injury.

The role of microbiota in concanavalin A-mediated liver injury

2018 ◽  
Vol 56 (01) ◽  
pp. E2-E89
Author(s):  
B Schiller ◽  
C Wegscheid ◽  
L Berkhout ◽  
A Zarzycka ◽  
U Steinhoff ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A

scholarly journals Reply to: “COVID-19-associated liver injury (COVALI): role of hepatologists”

2021 ◽  
Author(s):  
Dongxiao Li ◽  
Xiangming Ding ◽  
Dean Tian ◽  
Limin Xia
Keyword(s):  
Liver Injury

scholarly journals Liver Injury and the Macrophage Issue: Molecular and Mechanistic Facts and Their Clinical Relevance

2021 ◽  
Vol 22 (14) ◽  
pp. 7249
Author(s):  
Siyer Roohani ◽  
Frank Tacke
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Current Knowledge ◽  
Hepatocellular Cancer ◽  
Complete Recovery ◽  
Hepatic Macrophages ◽  
Liver Injuries ◽  
Microbial Products ◽  
Injured Liver

The liver is an essential immunological organ due to its gatekeeper position to bypassing antigens from the intestinal blood flow and microbial products from the intestinal commensals. The tissue-resident liver macrophages, termed Kupffer cells, represent key phagocytes that closely interact with local parenchymal, interstitial and other immunological cells in the liver to maintain homeostasis and tolerance against harmless antigens. Upon liver injury, the pool of hepatic macrophages expands dramatically by infiltrating bone marrow-/monocyte-derived macrophages. The interplay of the injured microenvironment and altered macrophage pool skews the subsequent course of liver injuries. It may range from complete recovery to chronic inflammation, fibrosis, cirrhosis and eventually hepatocellular cancer. This review summarizes current knowledge on the classification and role of hepatic macrophages in the healthy and injured liver.

scholarly journals An Unexpected Role of Cholesterol Sulfotransferase and its Regulation in Sensitizing Mice to Acetaminophen-Induced Liver Injury

2019 ◽  
Vol 95 (6) ◽  
pp. 597-605 ◽  
Author(s):  
Yunqi An ◽  
Pengcheng Wang ◽  
Pengfei Xu ◽  
Hung-Chun Tung ◽  
Yang Xie ◽  
...  
Keyword(s):  
Liver Injury

scholarly journals Depdc5 deficiency exacerbates alcohol-induced hepatic steatosis via suppression of PPARα pathway

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Lin Xu ◽  
Xinge Zhang ◽  
Yue Xin ◽  
Jie Ma ◽  
Chenyan Yang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Hepatic Steatosis ◽  
Liver Steatosis ◽  
Pharmacological Intervention ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Pathological Effect ◽  
Mtorc1 Pathway

AbstractAlcohol-related liver disease (ALD), a condition caused by alcohol overconsumption, occurs in three stages of liver injury including steatosis, hepatitis, and cirrhosis. DEP domain-containing protein 5 (DEPDC5), a component of GAP activities towards Rags 1 (GATOR1) complex, is a repressor of amino acid-sensing branch of the mammalian target of rapamycin complex 1 (mTORC1) pathway. In the current study, we found that aberrant activation of mTORC1 was likely attributed to the reduction of DEPDC5 in the livers of ethanol-fed mice or ALD patients. To further define the in vivo role of DEPDC5 in ALD development, we generated Depdc5 hepatocyte-specific knockout mouse model (Depdc5-LKO) in which mTORC1 pathway was constitutively activated through loss of the inhibitory effect of GATOR1. Hepatic Depdc5 ablation leads to mild hepatomegaly and liver injury and protects against diet-induced liver steatosis. In contrast, ethanol-fed Depdc5-LKO mice developed severe hepatic steatosis and inflammation. Pharmacological intervention with Torin 1 suppressed mTORC1 activity and remarkably ameliorated ethanol-induced hepatic steatosis and inflammation in both control and Depdc5-LKO mice. The pathological effect of sustained mTORC1 activity in ALD may be attributed to the suppression of peroxisome proliferator activated receptor α (PPARα), the master regulator of fatty acid oxidation in hepatocytes, because fenofibrate (PPARα agonist) treatment reverses ethanol-induced liver steatosis and inflammation in Depdc5-LKO mice. These findings provide novel insights into the in vivo role of hepatic DEPDC5 in the development of ALD.

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