ArticleMolecular medicine reports2020
Inhibition of HtrA2 alleviates inflammatory response and cell apoptosis in lipopolysaccharide‑induced acute pneumonia in rats.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Network-Based Integrated Analysis of Transcriptomic Studies in Dissecting Gene Signatures for LPS-Induced Acute Lung Injury.Inflammation · 2021Pooled it
- Leptospira interrogans HtrA protease is a potent inducer of multifaceted cellular responses.Antonie van Leeuwenhoek · 2026Article
- Xiaoxianxiong Decoction Attenuates LPS-Induced Pneumonia in Mice by Inhibiting Inflammatory Response Through Activation of SIRT1.FASEB bioAdvances · 2025Article
- UCF-101 ameliorates traumatic brain injury by promoting microglia M2 polarization via AMPK/NF-κB pathways in LPS-induced BV2 cells.Journal of molecular histology · 2024Article
- HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation.International journal of molecular sciences · 2024Review
- Role of high-temperature requirement serine protease A 2 in rheumatoid inflammation.Arthritis research & therapy · 2023Article
- PSMC2 knockdown inhibits the progression of oral squamous cell carcinoma by promoting apoptosis via PI3K/Akt pathway.Cell cycle (Georgetown, Tex.) · 2022Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Pneumonia is one of the commonest causes of death worldwide. High‑temperature requirement A2 (HtrA2) is a proapoptotic mitochondrial serine protease involved in caspase‑dependent or caspase‑independent cell apoptosis. UCF‑101 (5‑[5‑(2‑nitrophenyl) furfuryl iodine]‑1,3‑diphenyl‑2‑thiobarbituric acid), an inhibitor of HtrA2, has a protective effect on organs in various diseases by inhibiting cell apoptosis. The aim of the present study was to explore whether UCF‑101 has a protective effect on lungs in pneumonia. A lipopolysaccharide (LPS)‑induced pneumonia model was established in rats. UCF‑101 (2 µmol/kg) was used for treatment. Lung injury was detected by hematoxylin and eosin staining. Pro‑inflammatory cytokines and oxidative stress‑related factors were detected using corresponding test kits. TUNEL staining was used to measure the amount of cell apoptosis. Apoptosis‑associated proteins were detected by western blot assay. The present study indicated pulmonary injury induced by LPS. Treatment with UCF‑101 clearly alleviated this pulmonary damage and restored the levels of pro‑inflammatory cytokines and oxidative stress‑related factors. In addition, UCF‑101 significantly reduced LPS‑induced cell apoptosis, the release of HtrA2 and cytochrome from mitochondria to the cytoplasm and inhibited the expression of pro‑apoptotic proteins. UCF‑101 also restored the ATP level. The present results demonstrated that UCF‑101 acts as a positive regulator of acute pneumonia by inhibiting inflammatory response, oxidative stress and mitochondrial apoptosis. The present study suggests UCF‑101 as a potential candidate for pneumonia therapy.
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