ArticleJournal of molecular histology2025
Bevacizumab alleviates kidney damage by modulating inflammation, necroptosis and apoptosis: a preclinical study of renal ischaemia/reperfusion injury in rats.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal ischemia/reperfusion injury is a critical clinical problem caused by kidney and heart surgery and can lead to acute kidney injury (AKI). Bevacizumab is a humanized monoclonal antibody that binds to circulating soluble isoforms of VEGF-A, thereby inhibiting the activation of VEGF molecular pathways and eliciting antiangiogenic effects. This study assessed the nephroprotective potential of bevacizumab in a rat model of renal ischemia/reperfusion injury (I/R). Twenty-four Sprague-Dawley rats were allocated into four groups: Sham, I/R, I/R + normal saline, and I/R + bevacizumab. The sham group was subjected to laparotomy without I/R induction. The I/R, I/R + normal saline, and I/R + bevacizumab groups were subjected to 30 min of bilateral renal ischemia, followed by 24 h of reperfusion. The rats in the I/R + normal saline and I/R + bevacizumab groups were administered normal saline (vehicle for bevacizumab) and 0.1 mg/kg bevacizumab via intraperitoneal injection 60 min before ischemia, respectively. Renal damage markers (creatinine and KIM-1), inflammatory and oxidative markers (TNF-α, IL-1β, NF-κB, F8-isoprostane and SOD), and an apoptotic marker (caspase-3) were measured via ELISA. Nrf2 and MLKL were assessed by IHC, and RIPK1 and HO-1 were assessed by RT‒qPCR, in addition to histological examination and molecular docking. Compared with the sham group, the I/R and I/R + normal saline groups presented significant increases in creatinine, KIM-1, NF-κB, TNF-α, IL-1β, F8-isoprostane, caspase-3, RIPK1, and MLKL and a reduction in SOD. Compared with those in the sham group, the histological findings in the I/R and I/R + normal saline groups revealed notable structural damage. Conversely, bevacizumab significantly reduced renal damage, inflammatory marker levels, cellular death, and histopathological findings. In bevacizumab-treated rats, the nuclear translocation of Nrf2 and HO-1 increased. Moreover, molecular docking analysis revealed that bevacizumab interacted with Keap1. Bevacizumab has nephroprotective effects against renal IRI by diminishing inflammation, necroptosis, apoptosis, and necrosis through the activation of the Nrf2/HO-1 pathway and the inhibition of the RIPK1/MLKL pathway.
Indexed as
Identifiers
41123708What Socratic holds
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 Socratic graph.