Apocynum venetum Attenuates Acetaminophen-Induced Liver Injury in Mice

2015 ◽  
Vol 43 (03) ◽  
pp. 457-476 ◽  
Author(s):  
Wenyan Xie ◽  
Chen Chen ◽  
Zhihui Jiang ◽  
Jian Wang ◽  
Matthias F. Melzig ◽  
...  
Keyword(s):  
Liver Injury ◽  
Histopathological Examination ◽  
Folk Medicine ◽  
Analgesic Drug ◽  
Once Daily ◽  
Apocynum Venetum ◽  
Anti Oxidant ◽  
Underlying Mechanisms ◽  
Serum Aminotransferases ◽  
Hepatocyte Death

Apocynum venetum L. (A. venetum) has long been used in oriental folk medicine for the treatment of some liver diseases; however, the underlying mechanisms remain to be fully elucidated. Acetaminphen (APAP) is a widely used analgesic drug that can cause acute liver injury in overdose situations. In this study, we investigated the potential protective effect of A. venetum leaf extract (ALE) against APAP-induced hepatotoxicity. Mice were intragastrically administered with ALE once daily for 3 consecutive days prior to receiving a single intraperitoneal injection of APAP. The APAP group showed severe liver injury characterized by the noticeable fluctuations in the following parameters: serum aminotransferases; hepatic malondialdehyde (MDA), 3-nitrotyrosine (3-NT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH). These liver damages induced by APAP were significantly attenuated by ALE pretreatments. A collective analysis of histopathological examination, DNA laddering and western blot for caspase-3 and cytochrome c indicated that the ALE is also capable of preventing APAP-induced hepatocyte death. Hyperoside, isoquercitrin and their derivatives have been identified as the major components of ALE using HPLC-MS/MS. Taken together, the A. venetum possesses hepatoprotective effects partially due to its anti-oxidant action.

scholarly journals Lepidium meyenii Walp Exhibits Anti-Inflammatory Activity against ConA-Induced Acute Hepatitis

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Zheng ◽  
Shouwen Du ◽  
Mingyao Tian ◽  
Wang Xu ◽  
Yufei Tian ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Hepatitis ◽  
Suppressor Cells ◽  
Protective Effects ◽  
Traditional Herbal Medicine ◽  
Lepidium Meyenii ◽  
Serum Hormone ◽  
Underlying Mechanisms ◽  
Hepatocyte Death ◽  
Killer T Cells

Strong inflammation is a prominent pathogenesis of acute hepatitis, which can induce hepatocyte death and lead to liver failure. Lepidium meyenii Walp (Maca) is a traditional herbal medicine mostly used in improving sperm motility and serum hormone levels, etc. However, there are no reports that showed Maca was designed for treating hepatitis so far. Therefore, the protective effects and pharmacological mechanisms of Maca are unknown in hepatitis. In this study, we found that the protective effects of Maca extract ameliorate ConA-induced acute hepatitis (CIH) and underlying mechanisms. We determined that pretreatment with Maca extract significantly suppressed the production of aminotransferases and inflammatory cytokines, including IFN-γ, TNF-α, IL-1β, IL-2, IL-6, IL-12, and IL-17a, and moderated acute liver injury in CIH. Maca recruited more myeloid-derived suppressor cells (MDSCs) to the liver and suppressed infiltration of natural killer T cells (NKT cells) and macrophages in the liver. Furthermore, our data indicated the molecular mechanism of the inhibitory inflammatory effects of Maca, which should suppress the activation of NF-κB, IFN-γ/STAT1, and IL-6/STAT3 signalings. Collectively, this present research explores Maca as an effective hepatoprotective medicine to inhibit inflammation and liver injury caused by acute hepatitis.

scholarly journals Hepatoprotective activity of raspberry ketone is mediated via inhibition of the NF-κB/TNF-α/caspase axis and mitochondrial apoptosis in chemically induced acute liver injury

2019 ◽  
Vol 8 (5) ◽  
pp. 663-676 ◽  
Author(s):  
Dalia Fouad ◽  
Amira Badr ◽  
Hala A. Attia
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Cytochrome C ◽  
Dna Fragmentation ◽  
Liver Enzymes ◽  
Histopathological Examination ◽  
Hepatoprotective Activity ◽  
Raspberry Ketone ◽  
Tnf Α ◽  
Underlying Mechanisms

Abstract Raspberry Ketone (RK) is a natural phenolic compound which is marketed nowadays as a popular weight-reducing remedy, with reported antioxidant and anti-inflammatory activities. However, its biological activity is not fully elucidated. Hepatotoxicity is the leading cause of acute liver failure in Europe and North America, and its management is still challenging. Therefore, this study aimed to assess the therapeutic detoxification activity of RK against liver injury in vivo and to explore the underlying mechanisms using carbon tetrachloride (CCl4)-induced hepatotoxicity as a model. First, a dose–response study using 4 different doses, 25, 50, 100, and 200 mg kg−1 day−1, of RK was conducted. RK was administered for 5 days as a pretreatment, followed by a single dose of CCl4 (1 ml kg−1, 1 : 1 v/v CCl4 : olive oil). The RK dose of 200 mg kg−1 showed the greatest protective effect and was selected for further investigations. CCl4 hepatotoxicity was confirmed by elevation of liver enzymes, and histopathological examination. CCl4-induced oxidative stress was evident from increased lipid peroxidation measured as thiobarbituric acid reactive substances (TBARS) along with depleted superoxide dismutase (SOD), reduced glutathione (GSH), and total antioxidant capacity (TAC). Increased oxidative stress was associated with increased cytochrome c expression with subsequent activation of caspase-9 and caspase-3, in addition to DNA fragmentation reflecting apoptosis. CCl4 also induced the expression of inflammatory cytokines (NF-κB and TNF-α). Interestingly, RK hepatoprotective activity was evident from the reduction of liver enzymes, and maintenance of hepatocyte integrity and microstructures as evaluated by histopathological examination using H and E, and transmission electron microscopy. The antioxidant activity of RK was demonstrated by the increase of TAC, SOD, and GSH, with a concomitant decrease of the TBARS level. Moreover, RK pretreatment inhibited CCl4-induced upregulation of inflammatory mediators. RK antiapoptotic activity was indicated by the reduction of the expression of cytoplasmic cytochrome-C, a decrease of caspases, and inhibition of DNA fragmentation. In conclusion, this study demonstrates that RK is a promising hepatoprotective agent. The underlying mechanisms include antioxidant, anti-inflammatory, and anti-apoptotic activities. This is the first study reporting RK hepatoprotective activity in acute hepatic injury and approves its antiapoptotic effect in the liver.

scholarly journals Scutellarin Ameliorated Carbon Tetrachloride-Induced Chronic Liver Injury in Mice

2020 ◽  
Author(s):  
Zhimin Miao ◽  
Yingying Zhao ◽  
Chunyan Li ◽  
Lingmin Chen ◽  
Jianeng Zhou ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Function Analysis ◽  
Chronic Liver ◽  
Hepatoprotective Effect ◽  
Mrna Levels ◽  
Chronic Liver Injury ◽  
Tnf Α ◽  
Anti Oxidant ◽  
Underlying Mechanisms

Abstract Background: Erigeron breviscapus (Vant.) Hand. -Mazz. is an edible and traditional medical herb and its extract scutellarin (SCU) is a widely used flavonoid showing anti-oxidant and anti-inflammatory activities. The purpose of this study was to evaluate the hepatoprotective effect of SCU on carbon tetrachloride (CCl4)-induced chronic liver injury in mice and reveal the underlying mechanisms. Methods: Chronic liver injury in mice was induced by intraperitoneal injection of 1 ml/kg CCl4 every three days. SCU (15 mg/kg, 30 mg/kg and 60 mg/kg) was administered through gavage every day. Bifendate (120 mg/kg) serves as a positive drug to validate the effectiveness of SCU.Results: The hepatoprotective effect of SCU was confirmed by liver function analysis, histological analysis and TUNEL assay. Administration of SCU recovered the activities of superoxide dismutase (SOD) and reduced the production of malondialdehyde (MDA). Additionally, treatment with SCU significantly decreased the mRNA levels of pro-inflammatory cytokines including IL-6, IL-1β and TNF-α. Moreover, SCU treatment suppressed the activation of NF-κB by decreasing the degradation of IκBα and inhibited the expression of CYP2E1. The 16S rRNA sequencing demonstrated that intake of SCU significantly remodeled gut microbiota, especially enriching the following: Lactobacillus, Coprobacillus, Akkermansia, Bifidobacterium, Parabacteroides. Conclusion: Our findings showed that SCU effectively ameliorated CCl4-induced chronic liver injury. This hepatoprotective effects might be attributed to inhibition of CCl4-induced NF-κB and CYP2E1 activation and enrichment of beneficial microbial community.

scholarly journals Effect of the Total Extract of Averrhoacarambola (Oxalidaceae) Root on the Expression Levels of TLR4 and NF-κB in Streptozotocin-Induced Diabetic Mice

2015 ◽  
Vol 36 (6) ◽  
pp. 2307-2316 ◽  
Author(s):  
Xiaohui Xu ◽  
Tao Liang ◽  
Xing Lin ◽  
Qingwei Wen ◽  
Xingmei Liang ◽  
...  
Keyword(s):  
Body Weight ◽  
Histopathological Examination ◽  
Fasting Blood Glucose ◽  
Folk Medicine ◽  
Immunohistochemical Analysis ◽  
Tissue Expression ◽  
Pancreatic Tissue ◽  
Diabetic Mice ◽  
Total Extract ◽  
Expression Levels

Background: Averrhoacarambola L., which is a folk medicine used in diabetes mellitus (DM) in ancient China, has been reported to have anti-diabetic efficacy. Aims: The aim of this study was to evaluate the hypoglycemic effect of the extract of Averrhoacarambola L. root (EACR) on the regulation of the Toll-like receptor 4 (TLR4)-Nuclear-factor kappa B (NF-κB) pathway in B) pathway in streptozotocin (STZ)-induced diabetic mice. Methods: the mice were injected with STZ (120 mg/kg body weight) via a tail vein. After 72 h, the mice with FBG = 11.1 mmol/L were confirmed as having diabetes. Subsequently, the mice were treated intragastrically with EACR (300, 600, 1200 mg/kg body weight/d) and metformin (320 mg/kg body weight/d) for 14 days. Results: As a result the serum fasting blood glucose (FBG), interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) levels were decreased following EACR administration. Immunohistochemical analysis revealed that the pancreatic tissue expression levels of TLR4 and NF-κB were downregulated after EACR administration. EACR suppressed pancreatic mRNA expression level of TLR4 and blocked the downstream NF-κB pathway in the pancreas. According to Western blot analysis EACR suppressed pancreatic TLR4 and NF-κB protein expression levels. Histopathological examination of the pancreas showed that STZ-induced pancreas lesions were alleviated by the EACR treatment. Conclusion: These findings suggest that the modulation of the IL-6 and TNF-a inflammatory cytokines and the suppression of the TLR4-NF-κB pathway are most likely involved in the anti-hyperglycemic effect of EACR in STZ-induced diabetic mice.

scholarly journals Pengaruh Teknik dan Pelarut Ekstraksi Terhadap Aktivitas Antioksidan dari Empat Jenis Ekstrak Daun Rosella (Hibiscus sabdariffa L.)

2018 ◽  
Vol 1 (3) ◽  
pp. 014-019
Author(s):  
Ari Sri Windyaswari ◽  
Yenni Karlina ◽  
Amalia` Junita
Keyword(s):  
Free Radical ◽  
Folk Medicine ◽  
Water Extract ◽  
Ethanol Extract ◽  
Hibiscus Sabdariffa ◽  
Native Plant ◽  
Ic50 Values ◽  
Radical Method ◽  
Anti Oxidant ◽  
Infusion Method

Tanaman rosella merupakan tanaman asli dari benua Asia (India hingga Malaysia) dan benua Afrika. Kultivasi bagian bunga, daun, dan biji dari tanaman rosella (Hibiscus sabdariffa L.) telah lama digunakan oleh masyarakat sebagai bahan makanan dan pengobatan empiris. Hasil penelitian sebelumnya menunjukkan tanaman rosella memiliki aktivitas farmakologi sebagai antikanker, antibakteri dan antioksidan. Telah dilaporkan bahwa bagian daun dan akar rosella dilaporkan mengandung senyawa fenolik terbanyak dibandingkan dengan bagian lainnya. Penelitian ini bertujuan untuk mengetahui pengaruh teknik dan pelarut ekstraksi terhadap aktivitas antioksidan dari empat jenis ekstrak daun rosella (Hibiscus sabdariffa L.). Teknik ekstraksi yang dilakukan adalah maserasi, infus dan refluk menggunakan pelarut air dan pelarut etanol. Aktivitas peredaman radikal bebas DPPH teridentifikasi pada pola kromatogram lapis tipis dengan penampak bercak DPPH 0,2% dari seluruh ekstrak daun rosella. Pengujian aktivitas antioksidan menggunakan metode peredaman radikal bebas DPPH dilakukan terhadap seluruh ekstrak daun rosella, yaitu ekstrak air teknik maserasi (AM), ekstrak air teknik infus (AI), ekstrak etanol teknik maserasi (EM), serta ekstrak etanol teknik refluk (ER). Nilai IC50 ekstrak AM, AI, EM dan ER berturut-turut adalah: 0,00056 ppm (sangat kuat); 0,00057 (sangat kuat); 0,00044 ppm (sangat kuat); 0,00092 ppm (sangat kuat). Metode penyarian metabolit sekunder optimal untuk aktivitas antioksidan pada daun rosella adalah teknik ekstraksi maserasi dengan pelarut etanol (ER).   Rosella is one of a native plant from Asia (India to Malaysia) and Africa. The Flowers, leaves, and seeds cultivated from rosella (Hibiscus sabdariffa L.) have been used in folk medicine as food and empirical treatment.  The previous study reported the pharmacological activities of rosella as anti-cancer, anti-bacterial and anti-oxidant.  It has been reported that leaf and root of rosella found to have phenolic compounds as the major components. This research was conducted to evaluate the effect of extraction technique and solvent on the anti-oxidant activity of four extracts of rosella leaves (Hibiscus sabdariffa L.). The extraction techniques include maceration, infusion and reflux with water and ethanol. Scavenging activities of DPPF free radical of all rosella leaves extracts were identified by thin layer chromatography, indicated by DPPH 0,2% reagent. The evaluation of antioxidant activity using scavenging DPPH free radical method was performed to all rosella leaves extract, including water extract by maceration method (AM), water extract by infusion method (AI), ethanol extract by maceration method (EM), ethanol extract by reflux method (ER).  The IC50 values of AM, AI, EM and ER were 0,00056 ppm (very strong); 0,00057 (very strong); 0,00044 ppm (very strong); 0,00092 ppm (very strong). The most optimum method to extract secondary metabolite with anti-oxidant properties was maceration with ethanol (ER).

Rhizophora Mucronata Lam. (Mangrove) Bark Extract Prevents Ethanol-induced Liver Injury, Oxidative Stress and Apoptosis in Swiss Albino Mice

2021 ◽  
Author(s):  
Chitra Jairaman ◽  
Sabine Matou-Nasri ◽  
Zeyad I Alehaideb ◽  
Syed Ali Mohamed Yacoob ◽  
Anuradha Venkataraman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Histopathological Examination ◽  
Bark Extract ◽  
High Dose ◽  
Protective Effects ◽  
Rhizophora Mucronata ◽  
Ethanol Intoxication ◽  
Hepatoprotective Effects

Abstract The bark extract of Rhizophora mucronata (BERM) was recently reported for its prominent in vitro protective effects against liver cell line toxicity caused by various toxicants, including ethanol. Here, we aimed to verify the in vivo hepatoprotective effects of BERM against ethanol intoxication. An oral administration of different concentrations (100, 200, and 400 mg/kg) of BERM prior to high-dose ethanol via intraperitoneal injection was performed in mice. On the 7th day, liver and kidney sections were dissected out for histopathological examination. The ethanol intoxication caused large areas of liver necrosis while the kidneys were not affected. Pre-BERM administration decreased ethanol-induced liver injury, as compared to the mice treated with ethanol alone. In addition, the pre-BERM administration resulted in a decrement in the level of ethanol-induced oxidative stress, revealed by a concomitant increase of GSH and a decrease of MDA hepatic levels. The BERM extract also reversed the ethanol-induced liver injury and hepatotoxicity, characterized by the low detection of TNF-α gene expression level and fragmented DNA, respectively. Altogether, BERM extract exerts antioxidative activities and present promising hepatoprotective effects against ethanol intoxication. The identification of the related bioactive compounds will be of interest for future use at physiological concentrations in ethanol-intoxicated individuals.

scholarly journals Emodin promotes apoptosis of human endometrial cancer through regulating the MAPK and PI3K/ AKT pathways

2019 ◽  
Vol 13 (1) ◽  
pp. 489-496 ◽  
Author(s):  
Jun Jiang ◽  
Nanyang Zhou ◽  
Pian Ying ◽  
Ting Zhang ◽  
Ruojia Liang ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Signaling Pathways ◽  
Tumor Development ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Western Blot Assay ◽  
Anti Oxidant ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Dose Dependent

AbstractEmodin, a major component of rhubarb, has anti-tumor effects in a variety of cancers, influencing multiple steps of tumor development through modulating several signaling pathways. The aim of this study is to examine the effect of emodin on cell apoptosis and explore the underlying mechanisms in human endometrial cancer cells. Here we report that emodin can inhibit KLE cell proliferation and induce apoptosis in a time- and dose-dependent manner. Western blot assay found that emodin was involved in MAPK and PI3K/Akt signaling pathways. Specifically, emodin significantly suppressed the phosphorylation of AKT, and enhanced the phosphorylation of MAPK pathways. Furthermore, the generation of reactive oxygen species (ROS) was up-regulated in KLE cells upon treatment with emodin, while the anti-oxidant agent N-acetyl cysteine (NAC) can inhibit emodin-induced apoptosis and promote the activation of AKT and Bcl-2. Taken together, we revealed that emodin may induce apoptosis in KLE cells through regulating the PI3K/AKT and MAPK signaling pathways, indicating the importance of emodin as an anti-tumor agent.

scholarly journals A Discovery of Relevant Hepatoprotective Effects and Underlying Mechanisms of Dietary Clostridium butyricum Against Corticosterone-Induced Liver Injury in Pekin Ducks

2019 ◽  
Vol 7 (9) ◽  
pp. 358 ◽  
Author(s):  
Yanhan Liu ◽  
Cun Liu ◽  
Liqing Huang ◽  
Zhaofei Xia
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Liver Injury ◽  
Signaling Pathway ◽  
Basal Diet ◽  
Clostridium Butyricum ◽  
Pekin Ducks ◽  
Injury Model ◽  
Hepatoprotective Effects ◽  
Underlying Mechanisms

Clostridium butyricum (C. butyricum) can attenuate oxidative stress, inflammation, and hepatic fatty deposition in poultry, however, the underlying mechanisms for this in Pekin ducks remain unclear. This study evaluated these hepatoprotective effects and the underlying mechanisms in a corticosterone (CORT)-induced liver injury model in Pekin ducks fed a C. butyricum intervention diet. A total of 500 Pekin ducks were randomly divided into five groups: one group (CON group) was only provided with a basal diet, three groups were provided a basal diet with 200 mg/kg (LCB group), 400 mg/kg (MCB group), or 600 mg/kg (HCB group) C. butyricum, respectively, and one group was provided a basal diet with 150 mg/kg aureomycin (ANT group) for 42 d. At 37 days-old, all ducks received daily intraperitoneal injections of CORT for five days to establish a liver injury model. C. butyricum intervention alleviated liver injury by decreasing the liver organ indices, hepatic steatosis and hepatocyte necrosis, and improving liver function, antioxidant capacity, and inflammatory factors. Hepatic RNA-seq revealed 365 differentially expressed genes (DEGs) between the MCB and CON groups, with 229 up- and 136 down-regulated DEGs in the MCB group. Between the MCB and ANT groups, 407 DEGs were identified, including 299 up- and 108 down-regulated genes in MCB group. Some DEGs in the MCB group related to oxidative stress and inflammatory responses such as Sod3, Tlr2a/b, and Il10, which were up-regulated, while Apoa1, Cyp7a1, Acsl1/5, Fasn, Ppar-γ, and Scd, which are involved in lipid metabolism, were down-regulated, indicating that these genes were responsive to dietary C. butyricum for the alleviation of corticosterone-induced hepatic injury. Toll-like receptor signaling, PI3K-Akt signaling pathway, cytokine-cytokine receptor interaction, peroxisome proliferator-activated receptor (PPAR) signaling pathway, adipocytokine and glycerophospholipid metabolism signaling pathway were significantly enriched in the MCB group. These findings indicate that C. butyricum intervention can protect Pekin ducks from corticosterone-induced liver injury by the modulation of immunoregulatory- and lipid metabolism-related genes and pathways.

Epimedium koreanum Ameliorates Oxidative Stress-Mediated Liver Injury by Activating Nuclear Factor Erythroid 2-Related Factor 2

2018 ◽  
Vol 46 (02) ◽  
pp. 469-488 ◽  
Author(s):  
Ji Yun Jung ◽  
Sang Mi Park ◽  
Hae Li Ko ◽  
Jong Rok Lee ◽  
Chung A Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Hepg2 Cells ◽  
Liver Diseases ◽  
Caspase 3 ◽  
Glutathione Depletion ◽  
Related Factor ◽  
Nuclear Factor ◽  
Nrf2 Activation ◽  
Anti Oxidant

Oxidative stress induced by reactive oxygen species is the main cause of various liver diseases. This study investigated the hepatoprotective effect of Epimedium koreanum Nakai water extract (EKE) against arachidonic acid (AA)[Formula: see text][Formula: see text][Formula: see text]iron-mediated cytotoxicity in HepG2 cells and carbon tetrachloride (CCl4-)-mediated acute liver injury in mice. Pretreatment with EKE (30 and 100[Formula: see text][Formula: see text]g/mL) significantly inhibited AA[Formula: see text][Formula: see text][Formula: see text]iron-mediated cytotoxicity in HepG2 cells by preventing changes in the expression of cleaved caspase-3 and poly(ADP-ribose) polymerase. EKE attenuated hydrogen peroxide production, glutathione depletion, and mitochondrial membrane dysfunction. EKE also increased the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2), transactivated anti-oxidant response element harboring luciferase activity, and induced the expression of anti-oxidant genes. Furthermore, the cytoprotective effect of EKE against AA[Formula: see text][Formula: see text][Formula: see text]iron was blocked in Nrf2 knockout cells. Ultra-performance liquid chromatography analysis showed that EKE contained icariin, icaritin, and quercetin; icaritin and quercetin were both found to protect HepG2 cells from AA[Formula: see text][Formula: see text][Formula: see text]iron via Nrf2 activation. In a CCl4-induced mouse model of liver injury, pretreatment with EKE (300[Formula: see text]mg/kg) for four consecutive days ameliorated CCl4-mediated increases in serum aspartate aminotransferase activity, histological activity index, hepatic parenchyma degeneration, and inflammatory cell infiltration. EKE also decreased the number of nitrotyrosine-, 4-hydroxynonenal-, cleaved caspase-3-, and cleaved poly(ADP-ribose) polymerase-positive cells in hepatic tissues. These results suggest EKE is a promising candidate for the prevention or treatment of oxidative stress-related liver diseases via Nrf2 activation.

scholarly journals Evaluation of the relevance of DILI predictive hypotheses in early drug development: review of in vitro methodologies vs. BDDCS classification

2018 ◽  
Vol 7 (3) ◽  
pp. 358-370 ◽  
Author(s):  
Rosa Chan ◽  
Leslie Z. Benet
Keyword(s):  
Liver Injury ◽  
Drug Development ◽  
Safety Concern ◽  
Drug Induced ◽  
Development Review ◽  
Drug Induced Liver Injury ◽  
Underlying Mechanisms ◽  
Early Drug

Drug-induced liver injury (DILI) is a major safety concern; it occurs frequently; it is idiosyncratic; it cannot be adequately predicted; and a multitude of underlying mechanisms has been postulated.

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