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Updated: Aug 17, 2026
Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
Published on: January 3, 2025
The ischemic rat heart releases S100B
Guilherme S Mazzini1, Débora V Schaf, Alvaro R Oliveira
1Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul. Rua Ramiro Barcelos, 2600, anexo.CEP 90035-003. Porto Alegre, RS, Brazil.
Insights
The injured heart releases S100B, a protein previously used to detect brain injuries. This study confirms the ischemic heart as an extra-cerebral source of S100B, impacting its use as a specific neurological marker.
Area of Science:
- Biochemistry
- Cardiology
- Neurology
Background:
- S100B is an astrocytic protein used as a biomarker for cerebral injuries.
- Extra-cerebral sources may influence serum S100B levels.
- The injured myocardium has been reported to express S100B.
Purpose of the Study:
- To investigate whether the isolated heart releases S100B.
- To determine if myocardial ischemia and reperfusion lead to S100B release.
Main Methods:
- Isolated rat hearts were perfused using the Langendorff technique.
- Hearts were subjected to 20 minutes of ischemia followed by 30 minutes of reperfusion (ischemic group) or 50 minutes of perfusion (control group).
- Perfusion fluid was analyzed for S100B and cardiac troponin T levels at various time points.
Main Results:
- S100B and cardiac troponin T levels significantly increased in the ischemic group after reperfusion.
- Median S100B levels rose from <0.02 µg/L to 0.38 µg/L.
- Median troponin T levels increased from 0.31 µg/L to 2.84 µg/L.
Conclusions:
- The ischemic heart releases S100B.
- This finding identifies the heart as an extra-cerebral source of S100B.
- The results suggest that serum S100B levels may be influenced by cardiac injury.
Abstract:
S100B is an astrocytic protein assessed in cerebrospinal fluid and serum as a biochemical marker of cerebral injuries. However, increasing evidences suggest the influence of extra cerebral sources on its serum levels. Since it was reported that the injured myocardium expresses S100B, we investigated whether the isolated heart releases this protein. The rat hearts were excised and perfused by the Langendorff technique of isolated heart perfusion. After stabilization, 10 hearts (ischemic group) were submitted to 20 minutes of ischemia and 30 minutes of reperfusion, and 5 hearts (control group) were submitted to 50 minutes of perfusion. The perfusion fluid was collected at pre-ischemia, and 0, 5, 10, 15 and 30 min after ischemia (or equivalent in controls) for S100B and cardiac troponin T (a heart injury marker) assays. In the ischemic group, S100B and troponin T levels increased significantly at time 0 min: S100B values [mug/L, median (IQ25/IQ75)] increased from < or = 0.02 (< or = 0.02/0.03) to 0.38 (0.22/0.84), while troponin T values [mug/L, median (IQ25/IQ75)] increased from 0.31 (0.15/0.45) to 2.84 (2.00/3.63). Our results point to the ischemic heart as an extra cerebral source of S100B.
