Trial reportScientific reports2024
The impact of ulinastatin on lymphocyte apoptosis and autophagy in sepsis patients.
Trial report in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Corynoline promotes apoptosis and inhibits proliferation of glioblastoma via regulating the STAT3/Bcl-2 signalling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The interplay between type 2 diabetes mellitus and sepsis: a scoping review.International journal of medical sciences · 2026Article
- miR-1248 enhances bortezomib-induced autophagy by targeting MEF2C/p38-MAPK signaling in multiple myeloma.Frontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to assess the influence of ulinastatin (UTI) on lymphocyte apoptosis and autophagy in sepsis patients, as well as its effect on inflammatory factors and vital organ function, with the goal of providing insights for improved clinical management of sepsis. A total of 40 sepsis patients were randomly assigned to the UTI group or the control group. The UTI group received standard treatment plus intravenous UTI, while the control group received standard treatment alone. Peripheral blood samples were collected at multiple time points for analysis of lymphocyte apoptosis, autophagy, inflammatory markers, and organ function. Various experimental techniques including Hoechst staining, transmission electron microscopy, and Western blot analysis were utilized to assess lymphocyte apoptosis, autophagy, and related protein expression levels. The study revealed that UTI treatment significantly inhibited lymphocyte apoptosis and promoted autophagy in sepsis patients. The levels of autophagy-related proteins LC3-II and Beclin-1 were substantially elevated, while the ratio of anti-apoptotic Bcl-2 to pro-apoptotic Bax was increased following UTI treatment. Furthermore, the levels of inflammatory markers IL-6, procalcitonin, and C-reactive protein were markedly reduced in the UTI group compared to the control group. Additionally, UTI treatment led to improved liver, kidney and cardiac function as evidenced by reduced levels of liver enzymes and creatinine, and cardiac enzymes. The findings of this study demonstrate that UTI exerts a protective effect on septic patients by inhibiting lymphocyte apoptosis, promoting autophagy, and attenuating systemic inflammation. Moreover, UTI treatment was associated with improved liver, kidney, and cardiac function in septic patients. These results contribute to a better understanding of the clinical management of sepsis and underscore the potential of UTI as a therapeutic intervention in septic patients.
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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.