language English
Article 2024 · 18 atıf

Effect of tannic acid on doxorubicin-induced cellular stress: Expression levels of heat shock genes in rat spleen

Kizir, Duygu, Karaman, Melike, Demir, Yeliz, Ceylan, Hamid

Özet

Doxorubicin (DOX), an anthracycline group antibiotic, has been extensively employed as a potent chemotherapeutic agent for treating solid and hematopoietic tumors in humans. Amid exposure to diverse stress conditions, living organisms swiftly initiate the synthesis of heat shock proteins (HSPs), a set of highly conserved proteins. Tannic acid (TA) has garnered increasing study attention due to its special chemical properties, health benefits, and wide availability. This study's primary aim is to elucidate the impact of DOX and TA on the expression levels of Hsp90aa1, Hspa1a, Hspa4, and Hspa5 in the spleen tissues of rats. Sprague Dawley rats (Rattus norvegicus, male, 9-10 weeks old, 180 +/- 20 g) were randomly divided into 4 groups: control, DOX (30 mg/kg cumulative), TA (50 mg/kg), and DOX + TA (5 mg/kg and 50 mg/kg, respectively). Subsequently, spleen tissues were collected from rats, and complementary DNA libraries were generated after the application process. The quantitative real-time PCR method was used to detect and quantify the mRNA expression changes of the Hsp90aa1, Hspa1a, Hspa4, and Hspa5 genes our results showed that the mRNA expressions of the targeted genes were up-regulated in rat spleen tissues exposed to DOX. However, this increase was remarkably suppressed by TA treatment. These findings suggest that TA may serve as a protective agent, mitigating the toxic effects of DOX in the rat spleen.

Anahtar Kelimeler
doxorubicin heat shock proteins spleen tannic acid toxicity FAILURE HSP70 OVEREXPRESSION
WoS Kategorileri
Biochemistry & Molecular Biology Biotechnology & Applied Microbiology
Sürdürülebilir Kalkınma Amaçları
Künye
Dergi
BIOTECHNOLOGY AND APPLIED BIOCHEMISTRY
Yıl
2024
Cilt
71
Sayı
6
Sayfa
1339-1345
ISSN
0885-4513
eISSN
1470-8744
DOI
10.1002/bab.2633
WoS UID
WOS:001257897000001
Yayını aç (DOI)