American Journal of Biochemistry and Biotechnology

Carica papaya Fruit Attenuates Apoptotic Degeneration After Permanent Cerebral Ischemia Rat

Pratchaya Kaewkaen

DOI : 10.3844/ajbbsp.2018.255.261

American Journal of Biochemistry and Biotechnology

Volume 14, Issue 4

Pages 255-261


Apoptotic neurodegeneration is a phenomenon following cerebral ischemia. Both the increased caspase-3 and decreased Bcl-2 expression are reported to play crucial role on apoptosis in neuron. In addition, phytonutrient can successfully increase the endogenous antioxidant and lower the apoptotic responses. Therefore, anti-apoptotic effect of Carica papaya fruits was examined. To the best of our knowledge, no scientific effect was available. Therefore this study aimed to determine the effect of Carica papaya on neuron density and the densities of both caspase-3 and Bcl-2 immunopositive neuron in hippocampus. Adult male Wistar rats, weighing 280-320 g, were orally given Carica papaya fruits extract at doses of 50, 150 and 450 mg/kg at a period of 14 days before and 14 days after the occlusion of right Middle Cerebral Artery (Rt.MCAO). The results showed that Carica papaya fruits at high doses used in this study significantly attenuated the decreased neuron density in hippocampus. In addition, the high doses of Carica papaya could decrease caspase-3 immunopositive neuron density but increased density of Bcl-2 immunopositive neurons in hippocampus. The decreased caspase-3 immunopositive neuron density and the increased Bcl-2- immunopositive neurons might be partly responsible for neuroprotective effect of Carica papaya. Therefore, Carica papaya is the potential fruit to protect against apoptotic neurodegeneration following cerebral ischemia. However, further researches are essential to elucidate the possible mechanism.


© 2018 Pratchaya Kaewkaen. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.