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Crack Cocaine Smoke Induces Tissue Degeneration in Rat Submandibular Glands by Toll-like Signaling Pathway.

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Titel: Crack Cocaine Smoke Induces Tissue Degeneration in Rat Submandibular Glands by Toll-like Signaling Pathway.
Autoren: Avanci, Lorrany da Silva, de Souza, Daniel Vitor, de Aguiar, Gabriel Carvalhal, Guedes Pinto, Thiago, Rosario, Barbara dos Anjos, Viana, Milena de Barros, Ferreira, Yasmin Alaby Martins, Cordaro, Viviane Carlin, Pisani, Luciana Pellegrini, Ribeiro, Daniel Araki
Quelle: Pathophysiology; Sep2025, Vol. 32 Issue 3, p32, 11p
Schlagwörter: CRACK cocaine, SUBMANDIBULAR gland, HISTOPATHOLOGY, LABORATORY rats, AEROSOLS, CELL proliferation, TOLL-like receptors, DEGENERATION (Pathology)
Abstract: Background: This study investigated the impact of crack cocaine smoke exposure on the submandibular salivary gland of Wistar rats. Methods: The animals were distributed into four groups: control (CTRL); 25 mg exposure (CK25); 50 mg exposure (CK50); and 100 mg exposure (CK100). The animals were exposed to crack cocaine smoke once a day for five consecutive days. Results: Exposure to crack cocaine smoke-induced histopathological changes in submandibular salivary glands in all groups under exposure. The immunohistochemical analysis demonstrates that exposure to crack cocaine smoke led to an increase in BCL-2 and P16 expression in all groups exposed to crack cocaine (p < 0.05). The analysis of Ki-67 expression revealed a significant increase in immunoreactive cells across all exposure groups (p < 0.05). Although MYD88 expression was observed in all crack cocaine-exposed groups, only the group treated with the highest dose (100 mg) exhibited a statistically significant increase compared to the control group (p < 0.05). Conclusions: In summary, this study demonstrates that exposure to crack cocaine smoke-induced tissue degeneration in the submandibular salivary gland, increasing cellular senescence and promoting compensatory cell proliferation in Wistar rats. [ABSTRACT FROM AUTHOR]
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Datenbank: Complementary Index
Beschreibung
Abstract:Background: This study investigated the impact of crack cocaine smoke exposure on the submandibular salivary gland of Wistar rats. Methods: The animals were distributed into four groups: control (CTRL); 25 mg exposure (CK25); 50 mg exposure (CK50); and 100 mg exposure (CK100). The animals were exposed to crack cocaine smoke once a day for five consecutive days. Results: Exposure to crack cocaine smoke-induced histopathological changes in submandibular salivary glands in all groups under exposure. The immunohistochemical analysis demonstrates that exposure to crack cocaine smoke led to an increase in BCL-2 and P16 expression in all groups exposed to crack cocaine (p < 0.05). The analysis of Ki-67 expression revealed a significant increase in immunoreactive cells across all exposure groups (p < 0.05). Although MYD88 expression was observed in all crack cocaine-exposed groups, only the group treated with the highest dose (100 mg) exhibited a statistically significant increase compared to the control group (p < 0.05). Conclusions: In summary, this study demonstrates that exposure to crack cocaine smoke-induced tissue degeneration in the submandibular salivary gland, increasing cellular senescence and promoting compensatory cell proliferation in Wistar rats. [ABSTRACT FROM AUTHOR]
ISSN:09284680
DOI:10.3390/pathophysiology32030032