Imaging alkaline phosphatase activity in alcoholic liver disease via a rational-designed NIR fluorogenic probe.

Toward anti-bluing shift: A rationally designed photo-induced electron transfer-based polarity responsive lipid droplets-targeting fluorescent probe for real-time monitoring of drug-induced liver injury.

An ultralow-concentration, red-emissive dual-responsive fluorescent probe for real-time mitochondrial viscosity/polarity imaging.

Ultra-large Stokes-shifted NIR fluorescent probe for diagnosis of APAP-induced liver injury and its applications in food and bioimaging.

Novel strategies for identification and prevention of idiosyncratic liver injury caused by TCM compatibility: Exemplification by Epimedii Folium and Psoraleae Fructus.

Integration of network pharmacology, lipidomics, and transcriptomics analysis to reveal the mechanisms underlying the synergy between susceptibility factor TNF-α and Polygonum multiflorum-induced idiosyncratic liver injury in mice.

Dehydrocavidine alleviates lipopolysaccharide-induced acute liver injury by activating Nrf2 signaling pathway to inhibit hepatocyte ferroptosis.

Deficiency in beclin1 alleviates doxorubicin-induced liver injury through inhibiting ferroptosis and autophagy.

Yu Dan Tong Formula inhibits NLRP3 inflammasome activation by suppressing Ca²⁺ influx in treating cholestatic liver disease.

Disease-associated neutrophil heterogeneity in cancer therapy: Implications for precision immunotherapy.

Enhancement in the nutritional profile and hepatoprotective activity of pine pollen via Aspergillus niger fermentation.

Drug-induced liver injury (DILI) from acetaminophen (APAP) overdose involves ER stress, oxidative damage, apoptosis, and inflammation. This study assesses Terminalia arjuna bark extract (TAE) against APAP-induced toxicity in rats, comparing its efficacy with N-acetylcysteine (NAC) through key signaling and inflammatory markers. Twenty-four Wistar rats were equally divided into four groups: Control Negative (CN, no treatment), Control Positive (CP, acetaminophen 350 mg/kg), N-acetylcysteine (NAC, 150 mg/kg), and Terminalia arjuna bark extract (TAE, ethanolic, 80 mg/kg). Over 14 days, liver injury was induced in the CP group via acetaminophen, while the NAC and TAE groups received their respective treatments. Animals were decapitated on day 15, and biological samples were collected for analysis. Biochemical assessments included liver function markers (ALT, AST) and oxidative stress parameters (SOD, TAC, TBARS, TOS). Gene expression studies were performed for oxidative stress regulators (Keap1, Nrf2) and ER stress signaling molecules (ERK, JNK, PPAR-α, AKT). Histopathological examination evaluated liver architecture and cellular integrity. Acetaminophen induced significant hepatotoxicity, as reflected by elevated liver enzymes, increased oxidative stress, altered gene expression, and disrupted liver histology. APAP toxicity resulted in elevated oxidative stress, apoptosis, inflammation, and ER stress, leading to significant hepatic damage (p < 0.0001 vs CN). NAC and TAE treatments mitigated these effects, with TAE demonstrating superior improvement in oxidative stress markers (p < 0.0001 vs CP). Gene expression analysis revealed a protective shift in the Keap1-Nrf2 pathways in the treated groups. Histopathology confirmed reduced necrosis and preserved hepatic architecture in the NAC and TAE groups. T. arjuna exhibits potent hepatoprotective effects, comparable to NAC, through modulation of oxidative stress, apoptosis, and ER stress pathways. Further studies are needed to explore its clinical applicability in acute liver injury management.

Semen Sojae Praeparatum ameliorates triptolide-induced liver injury by regulating bile acid homeostasis and the Keap1/Nrf2/p62 axis.

Sector-specific ambient air pollution and biomarkers of liver injury. Findings of a cross-sectional population-based survey.

Gallic acid attenuates LPS-induced hepatic injury via SIRT-1-dependent immunomodulation and anti-apoptotic mechanisms in rats.

GPR132 drives macrophage M1 polarization and aggravates inflammation-associated liver injury.

Natural glycosides from Cistanche deserticola alleviate hepatic ischemia-reperfusion injury via a cAMP-mediated signaling pathway.

Pathological mechanisms of hepatic ischemia-reperfusion injury and stem cell-based therapeutic strategies: Mechanistic insights and translational perspectives.

Silencing OGFOD1 ameliorates hepatic ischemia-reperfusion injury through abrogating oxidative stress and apoptosis via downregulating SPARC.

Nuclear receptor ERRγ acts as a key transcriptional regulator of hepatic LCN2 expression in CCl4-induced acute liver injury.