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acetylcysteine

✓ Approved

Cumberland Pharmaceuticals Inc · 小分子 · 小分子

什么是 acetylcysteine？

acetylcysteine 是一种小分子，由Cumberland Pharmaceuticals Inc研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

公司Cumberland Pharmaceuticals Inc
药物类别小分子
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Cumberland Pharmaceuticals Inc

治疗适应症

acetylcysteine 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Hepatobiliary disordersHepatic function abnormal✓ Approved
Injury, poisoning and procedural complicationsToxicity to various agents✓ Approved

相关研究文献

PubMedJournal of translational medicine2026-06-13

Endothelial glycocalyx perturbation in obstructive sleep apnea is associated with repetitive hypoxemia and immunothrombotic endothelial dysfunction.

Müller Martin Bernhard MB, Kammerer Tobias T, Khan Humayun H, Schmid Annika A et al.

Obstructive sleep apnea (OSA) is associated with cardiovascular disease. The endothelial glycocalyx (eGCX) is a shear-sensitive intravascular barrier. The relevance of OSA and intermittent hypoxia (IH) for eGCX perturbation and cardiovascular disease in humans remains unclear. In a prospectively recruited observational cohort with cross-sectional biomarker analysis in men (n = 60), polysomnography quantified apnea-hypopnea index (AHI), oxygen desaturation index (ODI), and hypoxic burden (HB). Using single-time-point plasma sampling, eGCX glycosaminoglycans hyaluronan (HA) and heparan sulfate (HS) and the proteoglycan syndecan-1 (SDC-1) were related to OSA severity and repetitive hypoxemia, including multivariable adjustment for cardiometabolic, inflammatory, and renal determinants. Plasma proteomics defined pathways associated with OSA and HA/HS. Shear-matured primary human endothelial cells were exposed to OSA-characteristic IH cycles under arterial flow to assess eGCX structure, oxidative stress, nitric oxide (NO) signaling, thromboinflammatory status, and antioxidant treatment with N-acetylcysteine. Plasma HA and HS were higher in OSA than in non-OSA individuals and increased stepwise with disease severity, tracking AHI, ODI, and HB. These associations persisted in multivariable analyses adjusting for age, BMI, hypertension, hs-CRP, fasting glucose, and eGFR. Plasma SDC-1 did not differ between groups and remained non-associated in adjusted analyses. Proteomics revealed enrichment of inflammatory, coagulation, and oxidative stress-related pathways that strengthened with increasing OSA burden and higher HA/HS levels. Experimentally, IH caused loss of endothelial surface HA/HS with increased shedding, increased reactive oxygen species, reduced redox capacity, impaired NOS3/eNOS signaling and reduced NO bioavailability. IH or enzymatic eGCX digestion each enhanced monocyte and platelet adhesion, tissue factor expression, and fibrin deposition under shear, while N-acetylcysteine attenuated oxidative stress and partially restored surface HA expression. Integrated patient and IH-model data show that OSA severity and repetitive hypoxemia are associated with circulating markers consistent with eGCX perturbation, while the endothelial IH model supports induction of oxidative-inflammatory stress and a proadhesive, prothrombotic phenotype by intermittent hypoxia. Together, circulating HA and HS emerge as candidate biomarkers associated with OSA-related eGCX perturbation, warranting further evaluation in longitudinal and interventional studies of eGCX-stabilizing adjunct therapies. These findings derive from an all-male cohort and require validation in women and more diverse populations.

PMID 42286659
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PubMedAutophagy2026-06-13

STING1 senses mitochondrial damage to promote mitophagy.

Huang Ze-Bo ZB, Lin Jin-Yi JY, Cheng Ling-Jun LJ, Tan Hayden Weng Siong HWS et al.

The cGAS-STING1 pathway is essential for innate immunity, while its functions beyond immune activation have emerged as a key research topic. Recent studies have revealed the non-canonical roles of this pathway in autophagy. However, whether it participates in organelle quality control through selective autophagy processes such as mitophagy remains largely unexplored. In our study, we identify the cGAS-STING1 pathway as an essential upstream regulator of PINK1-PRKN-dependent mitophagy. We demonstrate that upon mitochondrial damage, STING1 is recruited to damaged mitochondria in a process requiring PINK1- and VCP/p97-mediated degradation of outer mitochondrial membrane proteins. STING1 at damaged mitochondria then activates TBK1, which phosphorylates the mitophagy receptor OPTN at Ser177, enhancing its recruitment to damaged mitochondria and driving efficient mitophagy. Disruption of the STING1-TBK1-OPTN axis impairs mitophagy and shifts the cellular response from pro-survival mitophagy to apoptosis. Our findings therefore uncover a non-canonical, pro-survival function of the cGAS-STING1 pathway in mitophagy, extending its role beyond innate immunity to the regulation of selective autophagy and cell fate decisions. Abbreviations: BafA1: bafilomycin A1; cGAS: cyclic GMP‑AMP synthase; ER: endoplasmic reticulum; GABARAP: GABA type A receptor-associated protein; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MQC: mitochondrial quality control; mtDNA: mitochondrial DNA; NAC: N-Acetylcysteine; Nec-1: Necrostatin-1; OMM: outer mitochondrial membrane; OPTN: optineurin; PINK1: PTEN induced kinase 1; PRKN: parkin RBR E3 ubiquitin protein ligase; RIPK1: receptor interacting serine/threonine kinase 1; ROS: reactive oxygen species; STING1: stimulator of interferon response cGAMP interactor 1; TBK1: TANK binding kinase 1; TFEB: transcription factor EB; VCP/p97: valosin containing protein; Z-VAD-FMK: benzyloxycarbony (Cbz)-l-ValAla-Asp (OMe)-fluoromethylketone.

PMID 42287086
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PubMedJournal of applied toxicology : JAT2026-06-13

Epirubicin Alters Pancreatic Autophagy and Insulin Synthesis Through a Zinc-Dependent Mechanism.

Afşar Ebru E, Eranıl Işıl I

Epirubicin (EPI) can cause metabolic side effects, including chemotherapy-related diabetes, partly through oxidative stress that disrupts zinc (Zn) homeostasis and impairs autophagy. This study investigated the effects of EPI on Zn regulation and autophagy in the pancreas, as well as the modulatory role of N-acetylcysteine (NAC). Rats received EPI (9.6 mg/kg) by intraperitoneal injection (i.p.) followed 1 h later by NAC (50 or 300 mg/kg, i.p.). Glucose homeostasis was assessed using the Homeostatic Model Assessment (HOMA-IR), and β-cell function was assessed using HOMA-β levels. Plasma insulin levels, as well as insulin, proinsulin, beclin, autophagy-related proteins (ATG5), Microtubule-Associated Protein 1 Light Chain 3 (LC3), phosphorylated Akt (p-Akt), mechanistic target of rapamycin complex 1 (mTOR1), cleaved caspase-3, Zrt/Irt-like Protein 10 (ZIP10), and the proliferation marker Ki-67 in pancreatic tissue, were measured using commercial ELISA kits. Total oxidant status (TOS) and total antioxidant status (TAS) were measured using commercial colorimetric assay kits, and the oxidative stress index (OSI) was calculated. Zn levels in pancreatic tissue and plasma samples were measured using a colorimetric method. Morphological changes in the pancreas were assessed by hematoxylin and eosin staining. As a result, in the EPI group, oxidative stress and ZIP10 levels increased, whereas Zn levels decreased, as well as pancreatic autophagy, proliferation, and insulin synthesis increased. Oxidative stress decreased in both the EN-50 and EN-300 groups, with a more pronounced decrease in the EN-300 group. Furthermore, in the EN-300 group, pancreatic Zn, ZIP10, autophagy, and proliferation levels decreased, whereas mTOR1 levels increased. The pancreatic insulin synthesis observed in the EN-50 group was not observed in the EN-300 group. In conclusion, the increased autophagy observed in the Epi group may reflect an adaptive response to oxidative stress. The effects of NAC on oxidative stress may be dose-dependent, and high-dose NAC administration may suppress EPI-induced autophagy via mTOR1-mediated signaling. Furthermore, the relationship among Zn levels, autophagy, and insulin synthesis observed in the experimental groups may contribute to a better understanding of EPI-associated diabetogenic alterations.

PMID 42286405
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PubMedGeneral physiology and biophysics2026-06-12

PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.

Ma Menghuai M, Liu Fan F, Yin Xiaomei X, Yue Jianhong J et al.

Atherosclerosis (AS) progression is closely linked to oxidized low-density lipoprotein (Ox-LDL)-induced endothelial cell injury. This study investigates the molecular mechanism by which the PCSK9 inhibitor Evolocumab (EVC) alleviates AS. We used Ox-LDL-induced HUVECs and high-fat diet (HFD)-fed ApoE-/- mice as in vitro and in vivo AS models. AS plaque formation was detected by HE and Oil Red O staining. The levels of lipid indicators and oxidative stress-related factors were measured via ELISA. The expression levels of PCSK9, apoptosis-related proteins, and signaling pathway-related proteins were determined via Western blotting. The result shows that EVC improved blood lipids and alleviated aortic injury in atherosclerotic mice, and concomitantly suppressed Ox-LDL-induced apoptosis and oxidative stress in HUVECs. In terms of the molecular mechanism, EVC attenuated the Ox-LDL-induced phosphorylation of ERK1/2, JNK and p38. Both the ROS inhibitor N-acetylcysteine and the p38 MAPK signaling pathway inhibitor SB203580 can enhance the suppressive effect of the PCSK9 inhibitor EVC on Ox-LDL induced apoptosis and oxidative stress in HUVECs, while the p38 MAPK signaling pathway activator C16-PAF shows the opposite results. In conclusion, the PCSK9 inhibitor EVC inhibits Ox-LDL-induced HUVECs apoptosis and oxidative stress by inhibiting the ROS/MAPK signaling pathway, thereby alleviating the progression of AS.

PMID 42281501
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PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-06-12

CRISPR screen identifies MAP2K3 as a key target for oleuropein to alleviate deoxynivalenol-induced hepatic injury.

Yang Yaqin Y, Wu Yue Y, Xu Xiaoqing X, Ihsan Awais A et al.

Deoxynivalenol (DON), a widely prevalent mycotoxin in temperate climates, causes significant hepatic injury upon the consumption of contaminated cereals. However, the key targets and mechanisms underlying DON-induced inflammatory hepatic injury remain unclear, thus hindering the development of targeted therapeutics. This study aimed to identify the key host targets mediating DON-induced inflammatory hepatic injury and its underlying molecular mechanism, as well as to discover potential therapeutic agents for alleviating this damage. We established a J774A.1-CRISPR-Cas9 whole-genome knockout library to screen for host genes essential for DON-induced apoptosis. Structure-based virtual screening was employed to identify MAP2K3 inhibitors, and the mechanism of oleuropein (Ole) action was explored using both in vivo and in vitro models. CRISPR screening revealed that MAP2K3 is crucial for DON-induced apoptosis. Mechanistically, MAP2K3 mediates inflammatory hepatic injury by activating the p38/p53/caspase-8/caspase-9/caspase-3 pathway. Virtual screening identified Ole as a direct MAP2K3 inhibitor, which binds to key amino acid residues (Lys149, Ser194, Tyr230). Ole effectively inhibited DON-induced hepatic damage in vitro. In the DON-induced murine hepatitis model, Ole demonstrated robust therapeutic effects against DON-induced hepatitis, and its efficacy was superior to that of N-acetylcysteine (NAC). This study demonstrates that MAP2K3 is a key target mediating DON-induced inflammatory hepatic injury and confirms oleuropein (Ole) as a potential therapeutic agent. Together, these findings advance our understanding of the underlying mechanisms and propose a new treatment strategy.

PMID 42275882
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PubMedNeurotoxicology2026-06-12

Mitochondria-driven oxidative stress mediates Cyproconazole-induced genotoxicity, caspase-dependent apoptosis, and glial neuroinflammation in Human neuronal and glial cell lines.

Asma Mnassri M, Hanen Chaabani C, Fatma Abderrazk A, Karima Rjiba R et al.

Cyproconazole (CYPRO), a triazole fungicide widely used in agriculture, poses potential risks to the central nervous system, yet its neurotoxic mechanisms remain poorly characterized. This study provides the first integrative mechanistic investigation of CYPRO-induced toxicity in two complementary human cell models: SH-SY5Y neuroblastoma and U87 glioblastoma cells. CYPRO reduced cell viability in a dose-dependent manner, with IC50 values of 100µM and 150µM for U87 and SH-SY5Y cells, respectively. Mechanistically, CYPRO triggered a collapse of the mitochondrial membrane potential (ΔΨm), driving mitochondrial superoxide accumulation and overwhelming enzymatic antioxidant defenses, as evidenced by elevated malondialdehyde levels and depleted superoxide dismutase and catalase activities. This oxidative burst directly induced DNA strand breaks (confirmed by Comet assay) and triggered G0/G1 cell cycle arrest, consistent with DNA damage checkpoint activation. The causal role of oxidative stress was established by N-acetylcysteine (NAC) rescue, which attenuated both genotoxicity and cytotoxicity. The resulting mitochondrial outer membrane permeabilization activated the intrinsic apoptotic pathway, culminating in caspase-3 activation and confirmed caspase-dependent cell death via Z-VAD-FMK rescue. In U87 glial cells, CYPRO further inhibited pro-survival PI3K/AKT signaling and induced a maladaptive MAPK remodeling, characterized by sustained ERK activation, progressive p38 attenuation, and ERK-driven c-Jun phosphorylation, while stabilizing IκB-α and suppressing canonical NF-κB responses. Crucially, despite NF-κB suppression, CYPRO-treated glial cells developed a robust neuroinflammatory phenotype evidenced by COX-2 cytoplasmic upregulation and biphasic TNF-α secretion, suggesting that alternative transcriptional mechanisms sustain inflammatory gene expression independently of the canonical NF-κB pathway. These findings reveal CYPRO as a neurotoxicant capable of simultaneously triggering cell-autonomous apoptosis and a glial neuroinflammatory response, and argue for the systematic inclusion of glial models in the neurotoxicological risk assessment of triazole fungicides.

PMID 42276258
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