Results 221 to 230 of about 380,993 (362)

Comprehensive dose-dependent hepatorenal protective effects of <i>Ziziphus nummularia</i> leaf extract against quinolphos-induced toxicity in Wistar rats. [PDF]

open access: yesFront Pharmacol
Rengaraj R   +7 more
europepmc   +1 more source

Pathophysiology and fate of hepatocytes in a mouse model of mitochondrial hepatopathies

open access: green, 2007
Francisco J. Díaz   +6 more
openalex   +2 more sources

Oral Celastrol Nanomedicine Targeting Intestinal Antigen‐Presenting Cells to Effectively Mitigate Autoimmune Uveitis via Gut‐Retina Axis

open access: yesAdvanced Science, EarlyView.
Oral nanoCEL exhibits effective intestinal targeting of antigen‐presenting cells and restores the Th17/Treg balance in lymph nodes and spleen, ultimately protecting the blood‐retinal barrier by inhibiting peripheral immune cell infiltration and suppressing retinal glial cell activation.
Jinrun Chen   +13 more
wiley   +1 more source

Selenoprotein H Functions as a PPARα Coactivator to Link Selenium Homeostasis to Hepatic Lipid Metabolism and Protect against Steatohepatitis

open access: yesAdvanced Science, EarlyView.
Our study identifies selenium deficiency as a hallmark of MASH pathogenesis. Dietary selenium supplementation enhances hepatic fatty acid oxidation (FAO) and attenuates MASH progression by activating the PPARα pathway via selenoprotein H (SELENOH). This selenium‐SELENOH‐PPARα nexus redefines the functional scope of selenoproteins, moving from redox ...
Yuwei Zhang   +11 more
wiley   +1 more source

Decoding hepatocyte ploidy [PDF]

open access: yesNature Reviews Gastroenterology & Hepatology, 2018
openaire   +2 more sources

ACSL1‐Dependent Microglial Lipoimmunometabolic Reprogramming Underlies Cognitive Deficits in Alcohol Use Disorder

open access: yesAdvanced Science, EarlyView.
This study reveals that chronic alcohol exposure selectively upregulates ACSL1 expression in prefrontal cortical microglia, driving lipid metabolism reprogramming and lipid droplet accumulation, which activates the NLRP3 inflammasome and sustains neuroinflammation. To reverse this process, a dual‐targeted lipid nanoparticle, siACSL1@LNP‐MR, is designed
Liang Hao   +8 more
wiley   +1 more source

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