ArticleInflammation2018
The Pannexin-1 Channel Inhibitor Probenecid Attenuates Skeletal Muscle Cellular Energy Crisis and Histopathological Injury in a Rabbit Endotoxemia Model.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 25 citations in OpenAlex.
- The impact of Panx1 on inflammation, immunity, and cancer: a comprehensive review.Frontiers in medicine · 2025Review
- Baicalin and probenecid protect against Glaesserella parasuis challenge in a piglet model.Veterinary research · 2024Article
- Pannexin1: insight into inflammatory conditions and its potential involvement in multiple organ dysfunction syndrome.Frontiers in immunology · 2023Review
- Hepatic pannexin-1 mediates ST2Clinical and translational medicine · 2022Article
- Role of Pannexin 1 ATP-Permeable Channels in the Regulation of Signaling Pathways during Skeletal Muscle Unloading.International journal of molecular sciences · 2021Article
- Probenecid Relieves Cerebral Dysfunction of Sepsis by Inhibiting Pannexin 1-Dependent ATP Release.Inflammation · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
This study aimed to investigate the effect of probenecid (Pro) as an inhibitor of the pannexin-1 (Panx-1) channel-mediated release of intracellular ATP to the extracellular compartment on inflammation, cellular energy crisis, and organ injury in a rabbit sepsis model induced by Escherichia coli lipopolysaccharides (LPS). A total of 24 anesthetized and ventilated rabbits were randomly assigned to receive one of four treatments: infusion of LPS without Pro (LPS group), infusion of LPS with Pro (LPS + Pro group), sham operation without Pro (normal group), and sham operation with Pro (normal + Pro group). The LPS group had significantly higher serum ATP levels, serum inflammatory factor levels (TNF-α, IL-6, and IL-1β), and lower ATP concentrations and ATP/ADP ratios in the skeletal muscle tissue than the normal group. Compared to that at baseline, the expression of Panx-1 in peripheral blood cells increased significantly after the infusion of LPS (fluorescence intensity of Panx-1: T0 (baseline) vs. T1 (post-LPS) = 10 ± 1.2 vs. 84 ± 48, P < 0.0001; paired differences 73 ± 46, P = 0.024). Moreover, the LPS group exhibited higher expression of Panx-1 in the skeletal muscle tissue than the normal group. The serum ATP level was significantly positively correlated with IL-1β (R = 0.602, P = 0.001), IL-6 (R = 0.381, P = 0.033), and TNF-α (R = 0.514, P = 0.005) in 24 paired measurements. Compared to the LPS group, the LPS + Pro group had significantly lower levels of inflammatory factors (TNF-α, IL-6, and IL-1β) and serum ATP. In the skeletal muscle tissue, the LPS + Pro group also had a higher ATP concentration (1.1 ± 0.15 vs. 1.33 ± 0.17, P = 0.041) and ATP/ADP ratio (0.37 ± 0.03 vs. 0.51 ± 0.06, P = 0.002) and a lower histopathological damage score (4.67 ± 0.52 vs. 3 ± 0.63, P = 0.004). An overexpression of Panx-1 channel might be responsible for the strong inflammatory response, high serum ATP level, and skeletal muscle cellular energy crisis and histopathological damages in sepsis. Inhibiting Panx-1 channel-mediated release of intracellular ATP could decrease the above-mentioned injuries, and Panx-1 might be a potential therapeutic target in sepsis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.