Open veterinary journal · 2025
Therapeutic effects of single-clove garlic extract on nicotine-induced inflammation and histopathological changes in rats.
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Yunita Maya Nurwartanti, Plumeriastuti Hani, Tyasningsih Wiwiek, Agustono Bodhi, Hardiono Andhika Lutfhi, Prasetyanuri Gabrian Wahyu, Shofia Shofia, Rahmaniar Reina Puspita, Rahman Md Aliar
Аннотация
BACKGROUND: Nicotine exposure causes cellular damage by generating reactive oxygen species, leading to inflammation. DNA damage, and diseases such as atherosclerosis. Single-clove garlic extract (SCGE) contains antioxidants such as allicin and flavonoids that may counteract nicotine's harmful effects by reducing pro-inflammatory cytokines, suggesting SCGE's potential as a natural therapeutic intervention to support good health.
AIM: This study aimed to investigate the effects of SCGE against nicotine-induced pneumotoxicity in rats by assessing its impact on TNF-α, interleukin 6 (IL-6), and structural integrity tracheal, pulmonary, and coronary artery tissues.
METHODS: The subjects of this study were 30 male rats which were divided into the following 5 treatment groups: T1 (negative control), T2 (3 mg/ml of nicotine), and T3 (3 mg/ml of nicotine and 3.6 mg/day vitamin C), T4; T5; T6 groups (3 mg/ml nicotine and 75; 100; 125 kg/mg body weight of SCGE). A nicotine exposure followed by oral SCGE was administered twice a day consecutively for 14 days. The TNF-α and IL-6 expression was evaluated using immunohistochemical staining. Histopathology of the tracheal and pulmonary organs and coronary arteries was performed using H&E staining.
RESULTS: The T4, T5, and T6 groups revealed that TNF-α and IL-6 levels were significantly lower than in T2 (2.90 and 4.72), reducing ciliary damage, epithelial height, and mucosal thickness. The T6 group exhibited significant differences in the coronary arteries (14.97 µm) compared with the T2 (121.36 µm). The mean lumen diameter of the coronary artery of the T4, T5, and T6 groups was increased compared with T2 (49.71 µm). Significant decreases (42,65%) were observed in hemorrhage, alveolar septal thickening, and inflammatory cell infiltration in the T6 compared to T2.
CONCLUSION: In conclusion, SCGE treatment can potentially mitigate pneumotoxicity caused by nicotine, as evidenced by improvements in TNF-α, IL-6, and histopathological damage of the tracheal, pulmonary, and coronary arteries. These findings suggest that SCGE could be explored as a potential natural therapeutic intervention for preventing or treating nicotine-induced lung damage. These findings suggest that SCGE could be explored as a potential natural therapeutic intervention to prevent or treat nicotine-induced lung damage. Further studies could explore the mechanisms underlying SCGE's anti-inflammatory and antioxidant properties.
AIM: This study aimed to investigate the effects of SCGE against nicotine-induced pneumotoxicity in rats by assessing its impact on TNF-α, interleukin 6 (IL-6), and structural integrity tracheal, pulmonary, and coronary artery tissues.
METHODS: The subjects of this study were 30 male rats which were divided into the following 5 treatment groups: T1 (negative control), T2 (3 mg/ml of nicotine), and T3 (3 mg/ml of nicotine and 3.6 mg/day vitamin C), T4; T5; T6 groups (3 mg/ml nicotine and 75; 100; 125 kg/mg body weight of SCGE). A nicotine exposure followed by oral SCGE was administered twice a day consecutively for 14 days. The TNF-α and IL-6 expression was evaluated using immunohistochemical staining. Histopathology of the tracheal and pulmonary organs and coronary arteries was performed using H&E staining.
RESULTS: The T4, T5, and T6 groups revealed that TNF-α and IL-6 levels were significantly lower than in T2 (2.90 and 4.72), reducing ciliary damage, epithelial height, and mucosal thickness. The T6 group exhibited significant differences in the coronary arteries (14.97 µm) compared with the T2 (121.36 µm). The mean lumen diameter of the coronary artery of the T4, T5, and T6 groups was increased compared with T2 (49.71 µm). Significant decreases (42,65%) were observed in hemorrhage, alveolar septal thickening, and inflammatory cell infiltration in the T6 compared to T2.
CONCLUSION: In conclusion, SCGE treatment can potentially mitigate pneumotoxicity caused by nicotine, as evidenced by improvements in TNF-α, IL-6, and histopathological damage of the tracheal, pulmonary, and coronary arteries. These findings suggest that SCGE could be explored as a potential natural therapeutic intervention for preventing or treating nicotine-induced lung damage. These findings suggest that SCGE could be explored as a potential natural therapeutic intervention to prevent or treat nicotine-induced lung damage. Further studies could explore the mechanisms underlying SCGE's anti-inflammatory and antioxidant properties.