ABSTRACT
Drug-induced liver injury (DILI) is an important clinical problem, which has received more attention in recent decades. It can be induced by small chemical molecules, biological agents, traditional Chinese medicines (TCM), natural medicines (NM), health products (HP), and dietary supplements (DS). Idiosyncratic DILI is far more common than intrinsic DILI clinically and can be classified into hepatocellular injury, cholestatic injury, hepatocellular-cholestatic mixed injury, and vascular injury based on the types of injured target cells. The CSH guidelines summarized the epidemiology, pathogenesis, pathology, and clinical manifestation and gives 16 evidence-based recommendations on diagnosis, differential diagnosis, treatment, and prevention of DILI.
Subject(s)
Chemical and Drug Induced Liver Injury/epidemiology , Cholestasis/chemically induced , Dietary Supplements/adverse effects , Liver Diseases/epidemiology , Anti-Bacterial Agents/adverse effects , Anti-Bacterial Agents/toxicity , Anti-Infective Agents/adverse effects , Anti-Infective Agents/toxicity , Chemical and Drug Induced Liver Injury/pathology , Chemical and Drug Induced Liver Injury/physiopathology , Chemical and Drug Induced Liver Injury/prevention & control , China/epidemiology , Cholestasis/complications , Cholestasis/pathology , Diagnosis, Differential , Dietary Supplements/toxicity , Drugs, Chinese Herbal/adverse effects , Female , Guidelines as Topic , Humans , Incidence , Liver Diseases/pathology , Liver Diseases/physiopathology , Liver Diseases/therapy , Male , Prognosis , Risk Factors , Severity of Illness IndexABSTRACT
OBJECTIVE: To study the effect of Chinese herbal compound (CHC) on the expression of hepatocyte cytochrome P450IIE1 in rat model of alcoholic fatty liver (AFL). METHODS: The AFL rats models were established by administering the drinking water with 40%(v/v) ethanol, and the changes of pathology in liver and hepatocyte P450IIE1 expression, as well as the contents of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), vitamin E (VitE) in liver were detected and compared with those in the control group. RESULTS: Fatty degeneration in liver recovered normally in the CHC-treated group. Immunohistochemical and in situ hybridization examination showed that CHC could inhibit the hepatocyte cytochrome P450IIE1 expression markedly, and restore the contents of MDA, SOD, GSH, VitE to nearly normal range. CONCLUSION: CHC can prevent AFL through inhibiting the hepatocyte cytochrome P450IIE1 expression markedly