Authors: Li, Yaling | Chandra, Thakur Prakash | Song, Xiong | Nie, Liangui | Liu, Maojun | Yi, Jiali | Zheng, Xia | Chu, Chun | Yang, Jun
Article Type:
Research Article
Abstract:
OBJECTIVE: We waimed to investigate whether H 2 S can relieve the myocardial fibrosis caused by doxorubicin through Keap1-Nrf2. METHODS: Sprague-Dawley (SD) rats were randomly divided into four groups: normal control group (Control); DOX model group (DOX); H 2 S intervention model group (DOX+H 2 S); H 2 S control group (H 2 S). DOX and DOX+H 2 S group were injected with doxorubicin (3.0 mg/kg/time) intraperitoneally. Both of the Control group and H 2
…S groups were given normal saline in equal volume, 2 weeks later, DOX+H 2 S and H 2 S group were controlled with NaHS (56 μ mol/kg/d) through the abdominal cavity, while the Control and DOX group were injected with normal saline of the same dosage intraperitoneally. RESULTS: Myocardial injury and myocardial cell apoptosis were significantly increased, the H 2 S content in myocardial tissue was remarkably down-regulated, the expression levels of MDA, Keap1, caspase-3, caspase-9, TNF-α , IL1β , MMPs and TIMP-1 in rat myocardial tissue was significantly up-regulated (P < 0.05), and the expression levels of GSH, NQO1, Bcl-2 were down-regulated compared with those of control group. The above results can be reversed by the DOX+H 2 S group. There is no statistically significant difference between the Control group and the H 2 S control group. CONCLUSIONS: These results suggest that H 2 S can improve DOX-induced myocardial fibrosis in rats, and the keap1/Nrf2 signaling pathway, oxidative stress, inflammation, and apoptosis may be involved in the mechanism.
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Keywords: Hydrogen sulfide, doxorubicin, myocardial fibrosis, keap1/Nrf2, apoptosis
DOI: 10.3233/THC-218020
Citation: Technology and Health Care,
vol. 29, no. S1, pp. 195-209, 2021