Abstract
Aims: The present study explored if pentraxin-3 (PTX-3) levels, which would be boosted due to cardiac damage by gentamicin, can be regressed thanks to Pycnogenol, which was also previously shown to have desirable impacts on cardiovascular diseases.
 Methods: In the study, we recruited 28 8-10-week-old male Sprague-Dawley rats into four groups: control, gentamicin, gentamycin+Pycnogenol, and Pycnogenol. We stained the tissue samples with hematoxylin-eosin and Masson’s trichome dye for histopathological analysis. Then, malondialdehyde (MDA) levels were measured using the spectrophotometric technique. In addition, we measured PTX-3 levels in the heart tissues by an immunohistochemical method.
 Results: We discovered the heart tissue samples of the rats in the control and Pycnogenol groups were histologically normal. As well as mononuclear cell increase and degeneration of cardiac muscle cells, we observed mild congestion in the gentamicin group compared to the control group. Despite more significant damage to the heart tissue in the gentamicin+Pycnogenol group compared to the control group, we found that the histopathological damage regressed in this group compared to the gentamicin group. While PTX-3 immunoreactivity was similar between the control and Pycnogenol groups, it was significantly elevated in the gentamicin group compared to the control group (p < 0.001). Moreover, the gentamicin+Pycnogenol group had decreased PTX-3 immunoreactivity than the gentamicin group. While MDA values followed a similar pattern between the control and Pycnogenol groups, these values were found to be significantly increased in the gentamicin group compared to the control group (p < 0.001). These values, however, were decreased in the gentamicin+Pycnogenol group compared to the gentamicin group.
 Conclusion: In a nutshell, the present study was able to demonstrate that gentamicin may lead to cardiac damage by boosting PTX-3 levels and that the damage can be regressed thanks to the Pycnogenol treatment.
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