ArticleCombinatorial chemistry & high throughput screening2026
Baihe Dihuang Danshen Decoction Alleviates Myocardial Ischemia-Reperfusion Injury in Depression-Induced Rats by Inhibiting Ferroptosis.
Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Ferroptosis in major depressive disorder: Molecular mechanisms, cellular vulnerability, and therapeutic opportunities.Biochemistry and biophysics reports · 2026Review
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7 authors.
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Abstract
introductionThe comorbidity of myocardial ischemia reperfusion injury (MIRI) and depression (DEP) may worsen the prognosis of coronary heart disease surgery. Currently, research on medications and therapeutic mechanisms for MIRI combined with DEP is still insufficient. This study aims to explore the relationship between DEP and MIRI, and the therapeutic effects and mechanisms of Baihe Dihuang Danshen decoction (BDDSD) on DEP combined with MIRI.
methodsSD rats were assigned to a final experimental framework of six groups (Sham, MIRI, DEP+MIRI, BDDSD, DEP drug control, MIRI drug control). DEP was induced via 6-week chronic unpredictable mild stress (CUMS), with BDDSD administered during the final 2 weeks. MIRI was then induced by 30-minute coronary artery ligation and 2-hour reperfusion. DEP severity was assessed using behavioral tests (open field, elevated plus maze, sucrose preference, forced swimming). MIRI outcomes were evaluated via infarct size, histopathology, serum markers (LDH, IL-6, IL-1β), myocardial oxidative stress (MDA, GSH, SOD, Fe
resultsCompared with the MIRI group, DEP significantly exacerbated MIRI, manifested by increased serum IL-6 and IL-1β levels, enlarged infarction area, and aggravated oxidative damage (elevated MDA/Fe DISCUSSION: DEP can aggravate inflammation and oxidative stress, promoting cardiac ferroptosis, thereby exacerbating MIRI. Our results demonstrate that BDDSD alleviates MIRI-DEP comorbidity through a dual mechanism, mitigating depressive symptoms and inhibiting myocardial ferroptosis via modulation of the NADPH/FSP1/CoQ10 pathway. Although the efficacy of BDDSD is encouraging, its dose-effect relationship and long-term safety require further study.
conclusionBDDSD effectively treats DEP-MIRI comorbidity through its dual mechanism, mitigating DEP and protecting against myocardial ferroptosis. Our study not only offers a novel therapeutic strategy for patients with DEP requiring coronary heart disease surgery but also provides new targets for developing drugs to treat MIRI combined with DEP.
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