Effects of exogenous thymosin β4 on carbon tetrachloride-induced liver injury and fibrosis.
Li X, Wang L, Chen C · Scientific reports · PMID 28724974
Study summary
Main finding
Thymosin beta4 attenuated liver-enzyme changes, tissue injury, collagen accumulation, and several inflammatory and oxidative-stress markers after chemical exposure.
Mice and rats exposed to carbon tetrachloride were used as models of acute liver injury and subsequent fibrosis.
What the researchers measured
Liver enzymes, oxidative-stress and inflammatory markers, collagen-related measures, and tissue damage were assessed.
How to read this evidence
Researchers studied cells, isolated tissue, or animals. These experiments can help explain a mechanism, but do not establish benefits or safety in people. Human cells grown in a laboratory also belong in this category.
Results in context
The findings concern chemically induced rodent injury. They do not establish prevention or reversal of liver fibrosis in people or outcomes with TB-500.
What this does not establish
Chemical rodent injury does not establish effects on human liver disease. Full-length thymosin beta4 results cannot be assigned to a product labeled TB-500 without verifying equivalence.
This collection includes related thymosin beta4 research. Parent or engineered peptide findings do not establish that a TB-500 fragment or a product sold under that name has the same effects.
Publication & source
Why this paper is included
The title focuses on thymosin beta4 or TB-500; parent-peptide findings do not establish TB-500 fragment effects.
Publication indexing
Journal Article · Research Support, Non-U.S. Gov't