ArticleBiochemistry and biophysics reports2026
Treating myocardial infarction combined with depression via regulating M1/TNF-α/TNFR1/NF-κB.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To further explore the underlying mechanism by which the traditional Mongolian medicine Anshen Buxin Liuwei Pills (ABLP) alleviates cardiac dysfunction and depressive behaviors in a model of myocardial infarction (MI) combined with depression. Method: Eighteen eight-week-old C57BL/6JNifdc male mice were divided into sham group (n = 6), MI + NS group (n = 6), MI + ABLP group (n = 6). Mice in the MI + ABLP group were treated with ABLP for 4 weeks. Seventeen eight-week-old wide-type (SERT Results: MI mice exhibited lower level of LVEF and LVFS than the sham mice, which were elevated by ABLP treatment. MI mice displayed depressive behaviors, as evidenced by a shorter total distance, slower speed, longer immobility time, shorter activity time, reduced center distance, shorter center time, decreased center entry times, shorter peripheral distance, decreased peripheral entry times, decreased sucrose water consumption and sucrose preference than the sham group (all P < 0.05); these behavioral deficits were rescued by ABLP administration. MI mice presented elevated levels of M1 cells, cardiac TNFR1, TNF-α, IKB-α and P65 proteins and TNFR1 mRNA expression, along with reduced TNFR2 proteins, relative to the sham group. ABLP significantly decreased the concentration of M1 cells, IKB-α, P65 (P < 0.05). Both the MI + NS and MI + ABLP groups had significantly higher level of cortex TNFR1, TNF-α, IKB-α, P65 proteins and TNFR1 mRNA expression, as well as lower level of cortex TNFR2 than the sham group (P < 0.05). There were no significant differences in serum hs-TNI, LVFS, LVEF, and SPT results among SERT Conclusion: ABLP treatment exerts beneficial effects in improving cardiac dysfunction and alleviating depressive behaviors in MI mice by inhibiting the M1/TNF-α/TNFR1/NF-κB signaling pathway. The underlying inflammatory response may be associated with cortical 5-HT levels.
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