ArticleInternational urology and nephrology2015
Augmenter of liver regeneration attenuates inflammation of renal ischemia/reperfusion injury through the NF-kappa B pathway in rats.
Article in International urology and nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Augmenter of liver regeneration protects the kidney against ischemia-reperfusion injury by inhibiting necroptosis.Bioengineered · 2022Article
- Augmenter of Liver Regeneration (ALR) Protects Kidney from Ischemia/Reperfusion (I/R) Injury via Regulation of TLR4/MAPK Signaling Pathway.Journal of immunology research · 2022Article
- Augmenter of liver regeneration ameliorates ischemia-reperfusion injury in steatotic liver via inhibition of the TLR4/NF-κB pathway.Experimental and therapeutic medicine · 2021Article
- Augmenter of Liver Regeneration Alleviates Renal Hypoxia-Reoxygenation Injury by Regulating Mitochondrial Dynamics in Renal Tubular Epithelial Cells.Molecules and cells · 2019Article
- Article
- Retracted Article: PVT1 knockdown alleviates vancomycin-induced acute kidney injury by targeting miR-124RSC advances · 2018Article
- The interplay of BMP4 and IL‑7 regulates the apoptosis of intestinal intraepithelial lymphocytes under conditions of ischemia̸reperfusion.International journal of molecular medicine · 2018Article
- Augmenter of liver regeneration: A fundamental life protein.Hepatology (Baltimore, Md.) · 2017Review
- Early protective role of MST1 knockdown in response to experimental diabetic nephropathy.American journal of translational research · 2016Article
- Magnesium isoglycyrrhizinate inhibits inflammatory response through STAT3 pathway to protect remnant liver function.World journal of gastroenterology · 2015Article
- Dexmedetomidine Inhibits TLR4/NF-κB Activation and Reduces Acute Kidney Injury after Orthotopic Autologous Liver Transplantation in Rats.Scientific reports · 2015Article
- Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation.Journal of translational medicine · 2015Article
- Exploring the Potential of Venom from Nasonia vitripennis as Therapeutic Agent with High-Throughput Screening Tools.Toxins · 2015Article
- Rosmarinic Acid Prevents Radiation-Induced Pulmonary Fibrosis Through Attenuation of ROS/MYPT1/TGFβ1 Signaling Via miR-19b-3p.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe effects of augmenter of liver regeneration (ALR) on the acute kidney injury (AKI) rats were investigated by measuring the inflammatory response associated with transcription factor nuclear factory (NF-κB) pathway.
methodsThe model of AKI rats was established by occluded the renal pedicles for 60 min and then released. After that, animals were treated with ALR (100 or 200 μg/kg). All rats were killed at different time points (24, 48, 72 h). Renal function and kidney histological changes were measured. The apoptosis of tubular cells was evaluated by TdT-mediated dUTP nick end labeling assay. Cytokines and chemokines were assessed by immunohistochemistry, enzyme-linked immunosorbent assay and real-time polymerase chain reaction (RT-PCR). The NF-κB p65 protein was analyzed by immunohistochemistry and RT-PCR, respectively.
resultsIschemia reperfusion induced tubular cells necrosis and apoptosis, and ALR can significantly reduce this damages. The productions of MCP-1, IL-1β and IL-6 were lower in the group of ALR treatment, especially in the high-dose group. The inflammatory infiltrates were lower in the rats with administration of ALR. ALR mediated the level of cytokines and chemokines through inhibited the activation of NF-κB.
conclusionALR can improve renal function and inhibit the expression of inflammatory factors. This protects against renal ischemia reperfusion injury, which may be associated with preventing NF-κB activation in rats.
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