Analysis of Renal Responses to Whole-body γ-Irradiation alone or Combined with Skin Injury Before the Onset of Renal Dysfunction in Mice DOI Open Access

Galeila Dawit,

Hong Wang,

Balamurugan Packialakshmi

и другие.

Опубликована: Июнь 11, 2024

The delayed effects of radiation alone and combined with skin injury on the kidney are poorly understood. We aimed to unravel compare inflammatory, oxidative stress, survival signaling pathways in cortex before mice manifested renal dysfunction after these two injuries. Mice were analyzed 30 days post irradiation (9.5 Gy for alone, 9.0 a wound). Radiation did not significantly alter BUN, NGAL, or KIM-1 protein levels, indicating preserved function. However, had increased nuanced effect health. activated distinct inflammatory pathways. STAT3-Y705 phosphorylation, while boosted STAT1-Y701 phosphorylation. Additionally, mRNA abundance IFNγR1, IFNγR2, heparanase IL-10, tended increase levels reduced IL-4 levels. Both injuries HO-1 protein, but also MnSOD catalase proteins. promoted AKT1-S473 phosphorylation diminished p53 suggesting inhibition apoptosis. In summary, despite activation stress pathways, both protective mechanisms such as AKT1, offering insights into molecular events manifesting dysfunction.

Язык: Английский

Astrocyte-derived exosomal miR-378a-5p mitigates cerebral ischemic neuroinflammation by modulating NLRP3-mediated pyroptosis DOI Creative Commons
Ruiting Sun,

Wenxin Liao,

Ting Lang

и другие.

Frontiers in Immunology, Год журнала: 2024, Номер 15

Опубликована: Авг. 8, 2024

This study aimed to investigate the regulatory role of astrocyte-derived exosomes and their microRNAs (miRNAs) in modulating neuronal pyroptosis during cerebral ischemia.

Язык: Английский

Процитировано

6
Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia–Reperfusion Injury DOI Creative Commons

Naranjan S. Dhalla,

Petr Ošťádal, Paramjit S. Tappia

и другие.

Antioxidants, Год журнала: 2025, Номер 14(3), С. 340 - 340

Опубликована: Март 14, 2025

Delayed reperfusion of the ischemic heart (I/R) is known to impair recovery cardiac function and produce a wide variety myocardial defects, including ultrastructural damage, metabolic alterations, subcellular Ca2+-handling abnormalities, activation proteases, changes in gene expression. Although I/R injury has been reported induce formation reactive oxygen species (ROS), inflammation, intracellular Ca2+ overload, generation oxidative stress considered play critical role development dysfunction. Increases production superoxide, hydroxyl radicals, oxidants, such as hydrogen peroxide hypochlorous acid, occur hearts subjected injury. In fact, mitochondria are major source excessive ROS due impairment electron transport system well xanthine oxidase NADPH oxidase. Nitric oxide synthase, mainly present endothelium, also activated injury, leading nitric oxide, which, upon combination with superoxide generates nitrosative stress. Alterations function, sarcolemma, sarcoplasmic reticulum activities, mitochondrial phosphorylation, protease simulated exposing oxyradical-generating (xanthine plus oxidase) or H2O2. On other hand, endogenous antioxidants dismutase, catalase, glutathione peroxidase, concentration transcription factor (Nrf2), which modulates expression various antioxidants, depressed hearts. Furthermore, pretreatment catalase N-acetylcysteine, mercaptopropionylglycerine observed attenuate I/R-induced handling Ca2+-regulatory activities; additionally, it found depress improve function. These observations indicate that intimately involved pathological effects different alterations Thus, we faced task developing safe effective agents for upregulating therapy

Язык: Английский

Процитировано

0
Exosome-related gene identification and diagnostic model construction in hepatic ischemia-reperfusion injury DOI Creative Commons

Yujuan You,

Shoulin Chen,

Binquan Tang

и другие.

Scientific Reports, Год журнала: 2024, Номер 14(1)

Опубликована: Сен. 28, 2024

Язык: Английский

Процитировано

3
CD11b-NOX2 mutual regulation-mediated microglial exosome release contributes to rotenone-induced inflammation and neurotoxicity in BV2 microglia and primary cultures DOI
Li Su, Ziyang Guo, Jianing Liu

и другие.

Free Radical Biology and Medicine, Год журнала: 2024, Номер 224, С. 436 - 446

Опубликована: Сен. 13, 2024

Язык: Английский

Процитировано

1
The Impact of Exosomes on Bone Health: A Focus on Osteoporosis DOI

Amir Mehrvar,

Mohammadarian Akbari,

Elaheh Mohandesi Khosroshahi

и другие.

Pathology - Research and Practice, Год журнала: 2024, Номер 263, С. 155618 - 155618

Опубликована: Сен. 30, 2024

Язык: Английский

Процитировано

1
Analysis of Renal Responses to Whole-body γ-Irradiation alone or Combined with Skin Injury Before the Onset of Renal Dysfunction in Mice DOI Open Access

Galeila Dawit,

Hong Wang,

Balamurugan Packialakshmi

и другие.

Опубликована: Июнь 11, 2024

The delayed effects of radiation alone and combined with skin injury on the kidney are poorly understood. We aimed to unravel compare inflammatory, oxidative stress, survival signaling pathways in cortex before mice manifested renal dysfunction after these two injuries. Mice were analyzed 30 days post irradiation (9.5 Gy for alone, 9.0 a wound). Radiation did not significantly alter BUN, NGAL, or KIM-1 protein levels, indicating preserved function. However, had increased nuanced effect health. activated distinct inflammatory pathways. STAT3-Y705 phosphorylation, while boosted STAT1-Y701 phosphorylation. Additionally, mRNA abundance IFNγR1, IFNγR2, heparanase IL-10, tended increase levels reduced IL-4 levels. Both injuries HO-1 protein, but also MnSOD catalase proteins. promoted AKT1-S473 phosphorylation diminished p53 suggesting inhibition apoptosis. In summary, despite activation stress pathways, both protective mechanisms such as AKT1, offering insights into molecular events manifesting dysfunction.

Язык: Английский

Процитировано

0