|
 
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| ORIGINAL ARTICLE |
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| Year : 2022 | Volume
: 6
| Issue : 3 | Page : 159-166 |
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Anti-Inflammation Relieving Heart Dysfunction and Depressive Behaviors of Mice Under Myocardial Infarction and Chronic Stress
Lijun Zhang1, Shuhui Tao2, Nan Lu3, Ruoyu Pan4, Meiyan Liu1
1 Department of Psycho-Cardiology, Beijing Anzhen Hospital Affiliated to Capital Medical University, Beijing, China
2 Department of Psycho-Cardiology, Beijing Anzhen Hospital Affiliated to Capital Medical University, Beijing; Department of Cardiology, Henan Medical School, Henan University, Kaifeng, China
3 Department of Cardiology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China
4 Department of Internal Medicine, School Hospital, Beijing Information Science and Technology University, Beijing, China
| Date of Submission | 27-Apr-2022 |
| Date of Acceptance | 11-Jul-2022 |
| Date of Web Publication | 30-Sep-2022 |
Correspondence Address:
Prof. Meiyan Liu
Department of Psycho-Cardiology, Beijing Anzhen Hospital Affiliated to Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing - 100 029
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/hm.hm_9_22
Background: Myocardial infarction (MI) induces high morbidity all over the world. Patients with MI are more vulnerable to depression, and depression worsens their prognosis. Inflammatory response is the primary pathophysiological mechanism of MI combined with depression. Therefore, MI and depression would benefit from attenuating inflammation. Objectives: To explore the anti-inflammation effect in relieving heart dysfunction and depressive behaviors of mice under MI and chronic stress. Materials and Methods: A total of 40 male C57BL/6J mice were given sham or MI surgery, and the success rate of the surgery was 80%. Hence, 32 mice survived surgery and were distributed as 8 in each group of study. Then, unpredictable chronic mild stress (UCMS) or Anshen Buxin Liuwei pills (ABL pills) group were applied to some MI mice, and the mice were divided into different groups, including sham group, MI group, MI + UCMS group, and MI + UCMS + ABL pills group (n = 8). After a 2-week treatment, the mice underwent the sucrose preference test, and echocardiography before sacrifice. Then, the mice were sacrificed for pathological detection and inflammatory cytokines detection. Results: Compared with mice in the sham group, those mice had lower left ventricular ejection fraction (LVEF) (51.25 ± 9.92 vs. 12.18 ± 8.46, 20.95 ± 16.40, 29.55 ± 13.33%, P < 0.05) and left ventricular fractional shortening (LVFS) (21.12 ± 6.82 vs. 5.57 ± 4.0, 9.89 ± 8.03, 14.0 ± 6.65%, P < 0.05) in the MI, MI + UCMS, and MI + UCMS + ABL pills groups. ABL pills could reverse cardiac dysfunction for the significant elevation of LVEF and LVFS. The hematoxylin and eosin staining presented left ventricular (LV) enlargement, inflammatory cell infiltration, and myocardial fibrosis formation in MI and MI + UCMS mice. While ABL pills reversed the pathological changes induced by ligation of the left anterior descending. The enzyme-linked immunosorbent assay detection showed that MI and MI + UCMS elevated the concentrations of cardiac tumor necrosis factor-α (TNF-α) and tumor necrosis factor receptor 1 (TNFR1), which were reduced by ABL pills. ABL pills significantly reversed the depressive behaviors of mice with MI + UCMS (82.97 ± 3.04 vs. 76.07 ± 7.84%, P < 0.05). MI + UCMS group had a higher level of cortex TNFR1 than sham and MI, while ABL pills reversed the elevation (P > 0.05). Conclusions: Anti-inflammation treatment effectively improves cardiac function and depressive behaviors via inhibiting TNF-α/TNFR1.
Keywords: Anti-inflammation, chronic stress, depressive behaviors, myocardial infarction, tumor necrosis factor-α
How to cite this article:
Zhang L, Tao S, Lu N, Pan R, Liu M. Anti-Inflammation Relieving Heart Dysfunction and Depressive Behaviors of Mice Under Myocardial Infarction and Chronic Stress. Heart Mind 2022;6:159-66 |
How to cite this URL:
Zhang L, Tao S, Lu N, Pan R, Liu M. Anti-Inflammation Relieving Heart Dysfunction and Depressive Behaviors of Mice Under Myocardial Infarction and Chronic Stress. Heart Mind [serial online] 2022 [cited 2023 Jun 10];6:159-66. Available from: http://www.heartmindjournal.org/text.asp?2022/6/3/159/357555 |
| Introduction | |  |
Myocardial infarction (MI) induces high morbidity all over the world. In China, the morbidity of acute MI (AMI) is 784.7/million in rural area and 623.3/million in urban area reported by the nearest “Report on Cardiovascular Health and Diseases Burden in China.”[1] MI could lead to ischemia-reperfusion injury, adverse cardiac remodeling, heart failure-related quality-of-life impairment,[2] and poor prognosis.[3] Despite drug therapy, percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) are vital managements for MI. While studies report that patients with PCI or CABG have a high prevalence of depression.[4],[5]
There is a close and bidirectional association between depression and MI.[6],[7] Depression links with thrombotic risk and arterial events, which could initiate AMI;[8] moreover, depression increases cardiovascular complications and long-term mortality in patients with post-AMI.[9] Approximately 15%–30% of patients with coronary heart disease (CHD) suffer from depression, especially those with MI who are more vulnerable to depression.[10] Smolderen et al. show that AMI patients with untreated depression are at higher risk of poor prognosis and mortality.[11] Therefore, a better understanding of the mechanisms of the comorbidity would benefit MI and depression management.
The potential pathophysiological mechanisms of MI combined with depression involve inflammatory response, the dysfunction of 5-hydroxytryptamine (5-HT) system, and the imbalance of hypothalamus-pituitary-adrenal (HPA) axis function and so on.[6],[12] The increasing inflammatory cytokines influence the metabolism of 5-HT and contribute to the reduction of 5-HT in the synaptic cleft, leading to depression.[13] Several clinical studies, such as the Canakinumab anti-inflammatory thrombosis outcome study trial,[14] the colchicine cardiovascular outcomes trial[15] and the low-dose colchicine trial,[16] have confirmed that administering anti-inflammatory drugs is beneficial for coronary revascularization, preventing major adverse cardiovascular events in patients with CHD. Furthermore, our former studies have shown inflammation participated in the depressive behaviors of the mice post-MI, and anti-inflammatory treatment could attenuate the depressive behaviors.[17] Tumor necrosis factor-α (TNF-α) takes part in the pathophysiological mechanisms of depression for inducing HPA axis activation and 5-HT dysfunction.[18] Hence, anti-inflammatory therapy would be promising to improve cardiac function and depressive behaviors.
Some studies exploring the effect of natural medicines present the anti-inflammatory effect of natural drugs can relieve depression post-MI. In the former study, we found that Anshen Buxin Liuwei pills (ABL pills),[19] a kind of Mongolian natural medicine, could attenuate depressive behaviors in mice under chronic stress by reducing inflammatory cytokine levels, such as interleukin-18 (IL)-18. Moreover, clinical practices have also proved the effectiveness of ABL pills in relieving angina. However, further studies need to be conducted. Thus, we perform this study to explore the anti-inflammation effect of ABL pills in relieving heart dysfunction and depressive behaviors of mice under MI and chronic stress.
| Materials and Methods | | |
A total of 40 male C57BL/6J mice specific pathogen-free (SPF (Beijing) Biotechnology Co., Ltd., No. 110324210106108525) were housed in the SPF laboratory. The mice were 8 weeks old and weighed 20–25 g. The environment was comfortable for adaption, with 12-h light-dark cycle, food and water ad libitum (room temperature, 20–23°C; humidity, 55%–65%). After adaptation for 3 days, the mice were given sham or MI surgery. The details of MI surgery were described in the following section. Thirty-two mice survived surgery and were distributed as 8 in each group of study; the mice were housed for recovery for 4 days. Then the mice were divided into four groups, including the sham group, MI group, MI + UCMS group, and MI + UCMS + ABL pills group. After a 2-week treatment, the mice underwent the sucrose preference test (SPT), and echocardiography before sacrifice. Then, the mice were sacrificed for pathological detection and inflammatory factors detection. After fasting for 10 h, the mice were anesthetized by injecting 0.3% pentobarbital sodium and then sacrificed. The blood, heart, brain, and spleen were collected for the experiments as described in [Figure 1].
This experiment earnestly obeyed the animal care guidelines formulated by the Institute for Laboratory Animal Research of Capital Medical University affiliated Beijing Anzhen Hospital. The experiment was approved by the Animal Ethical and Welfare Committee of Capital Medical University, affiliated with Beijing Anzhen Hospital (No. 2019036X).
MI surgery
The mice were deeply anesthetized by 2% isoflurane, 1 L/min pure oxygen (Small animal anesthesia machine, VETEQUIP, VE3525). The mice were kept warm and placed supinely. After preparing the skin and applying the electrocardiogram (ECG) monitor for recording ECG before and after the surgery, the heart was exposed, and the left anterior descending (LAD) coronary artery was ligated fast by 6–0 chorda serica chirurgicalis sterilis. When the infarcted zone turned white, the thoracic cavity was closed soon. The MI positive criteria included: the infarcted area turned white; the ECG showed apparent ST-segment elevations.
Sham surgery
The process of sham surgery was the same as MI surgery except for LAD ligation.
Unpredictable chronic mild stress
Four kinds of unpredictable chronic mild stress (UCMS) were applied to the mice in MI + UCMS group and MI + UCMS + ABL pills group, including 45° incline for 30 min, sound stress for 30 min, no bedding for 24 h, and wet bedding for 24 h. The same kind of stress appeared once every 4 days.
Drug treatment
Mice in the sham, MI, and MI + UCMS groups were treated with saline for two consecutive weeks. Mice in the MI + UCMS + ABL pills group were treated with ABL pills (Wulan Haote Zhongmeng Pharmacy Co., Ltd) at 0.6 g/kg/d for two consecutive weeks.[15],[20]
Echocardiography
Before echocardiography, the mice were deeply anesthetized by 2% isoflurane, 1 L/min pure oxygen (Small animal anesthesia machine, VETEQUIP, VE3525). Then, echocardiography was performed to measure left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular (LV) mass, LV mass correction (Visualsonics Vevo 2100 with 20 MHz linear transducer).
Sucrose preference test
The depressive behaviors of the mice were evaluated by SPT after 2-week treatment. The process of SPT was described in our former study.[21] Each mouse was kept alone in one cage. The cage was placed a bottle of pure water on one side and a bottle of 0.5% saccharine on the other side. The mice were kept for sucrose adaptation for 24 h. The place of the bottle was changed for 12 h. Then the SPT continued for another 24 h. The weights of the bottles were recorded before and after the experiment. The sucrose preference was calculated by (sucrose consumption/total water consumption) ×100%.
Flow cytometry
The spleens were collected for flow cytometry (Beckman CytoFLEX S, Beckman Coulter, CA, USA). The method of intracellular staining (Aqua+CD4+CD3+IL-4+Interferon [IFN]-γ) was used to present the expression of CD4+ T helper (Th) cells (Th1 and Th2), and the antibodies included (PE anti-mouse CD4, No. 100511; FITC anti-mouse CD3, No. 100305; APC anti-mouse IL-4, No. 504105; Brilliant Violet 421™ anti-mouse IFN-γ, No. 505829; BioLegend, USA). The method of intranuclear staining (Aqua+CD4+CD3+CD25+FOXP3) was applied to present the expression of regulatory Th cells (Treg), and the antibodies involved (Brilliant Violet 421™ anti-mouse CD25, No. 102033; PE anti-mouse CD4, No. 100511; FITC anti-mouse CD3, No. 100305; Alexa Fluor® 647 anti-mouse/rat/human FOXP3; BioLegend, USA) [Table 1].
Enzyme-linked immunosorbent assay
The serums were detected for N-terminal B-type natriuretic peptide (NT-proBNP) (MM-0558M1, Jiangsu Meimian Industrial Co., Ltd, Jiangsu, China). The cardiac tissues and cortex tissues were detected for TNF-α (INS202412M, Inselisa, Huangshi, Hubei, China), tumor necrosis factor receptor 1 (TNFR1) (MM-45934M1, Jiangsu Meimian Industrial Co., Ltd, Jiangsu, China). All the process of the enzyme-linked immunosorbent assay (ELISA) detection was conducted according to the instruments of the ELISA Kits [Table 1].
Hematoxylin and eosin staining
The pathological changes in the hearts were shown by hematoxylin and eosin (HE) staining. There were three main steps: specimens fixation, hematoxylin staining, eosin staining, dehydration, and sealed. Then, the panoramic scanner was used for HE staining sections scanning (Pannoramic DESK/MIDI/250/1000) and reading (Case Viewer 2.4, 3Dhistech, Hungary).
Statistical analysis
In this study, the data were presented as mean ± standard deviation (SD) for normal distribution. In the group comparisons of sham, MI, MI + UCMS, MI + UCMS + ABL pills, one-way ANOVO, and post-hoc test were applied. Least significant differences were used, such as SPT comparison. Two-tailed P < 0.05 was considered to be statistically significant. The software of SPSS 24.0 (SPSS Inc., Chicago, IL, USA) and GraphPad Prism 8 (USA, San Diego, CA) were used for data analysis.
| Results | | |
Cardiac dysfunction be reserved via reducing cardiac tumor necrosis factor-α/tumor necrosis factor receptor 1
In the group comparisons of serum NT-proBNP, there was no significant differences among the four groups (P > 0.05) [Figure 2]a. There were significant differences in cardiac function among the four groups [Figure 2]b, [Figure 2]C, [Figure 2]d. Compared with mice in the sham group, those mice had lower LVEF (51.25 ± 9.92 vs. 12.18 ± 8.46, 20.95 ± 16.40, 29.55 ± 13.33%, P < 0.05) and LVFS (21.12 ± 6.82 vs. 5.57 ± 4.0, 9.89 ± 8.03, 14.0 ± 6.65%, P < 0.05) in the MI, MI + UCMS, and MI + UCMS + ABL pills groups [Figure 2]b. While ABL pills could reverse cardiac dysfunction by elevating the value of LVEF and LVFS significantly. Compared with the sham mice, MI surgery had also caused a decrease of LV mass (103.06 ± 11.36 vs. 70.86 ± 15.70 mg, P < 0.05; 103.06 ± 11.36 vs. 86.04 ± 34.46, P > 0.05; 103.06 ± 11.36 vs. 91.91 ± 27.14 mg, P > 0.05) and LV mass correction (82.44 ± 9.09 vs. 56.69 ± 12.56 mg, P < 0.05; 82.44 ± 9.09 vs. 68.83 ± 27.57 mg, P > 0.05; 82.44 ± 9.09 vs. 73.53 ± 21.71 mg, P > 0.05) in the MI, MI + UCMS, and MI + UCMS + ABL pills groups. ABL pills could increase LV mass and LV mass correction without significance [Figure 2]c. | Figure 2: The cardiac function: (a) Group comparisons of serum NT-proBNP; (b) Group comparisons of LVEF and LVFS; (c) Group comparisons of LV mass and LV mass C; (d) M model of echocardiography, LVEF = Left ventricular ejection fraction, LVFS = Left ventricular fractional shortening, NT-proBNP = N-terminal B-type natriuretic peptide
Click here to view |
After the mice were executed, the hearts were taken out. We could see the apparent infarct area of the heart after MI [Figure 3]a. The HE staining presented LV enlargement, inflammatory cell infiltration, and myocardial fibrosis formation in MI and MI + UCMS mice. While ABL pills reversed the pathological changes induced by ligation of LAD [Figure 3]b. The ELISA detection showed that MI and MI + UCMS elevated the concentrations of cardiac TNF-α and TNFR1, which were reduced by ABL pills [Figure 3]c. Therefore, it was considered that the ABL pills could improve cardiac function by reducing cardiac TNF-α/TNFR1. | Figure 3: Infarcted heart and inflammation: (a) The heart specimens of the four groups; (b) HE staining of the hearts; (c) Group comparisons of TNF-α and TNFR1, TNF-α = Tumor necrosis factor-α, TNFR1 = Tumor necrosis factor receptor 1
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To explore the cell origin of the inflammatory factors, we performed flow cytometry to detect the spleens' immune cells (Treg, Th1, and Th2). However, there was no significance in the comparisons of Treg, Th1, and Th2 among the four groups [Figure 4]. | Figure 4: Group comparisons of Treg, Th1, and Th2, Th=T helper; Treg=regulatory Th cells
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Depressive behaviors were attenuated via reducing cortex tumor necrosis factor-α/tumor necrosis factor receptor 1
The SPT presented that mice under both MI and UCMS had a lower sucrose preference ratio which indicated depressive behaviors. ABL pills significantly reversed the depressive behaviors of mice with MI + UCMS (82.97 ± 3.04 vs. 76.07 ± 7.84%, P < 0.05) [Figure 5]a. | Figure 5: Depressive behaviors and cortex inflammation. (a) Group comparisons of sucrose preference test; (b) Group comparisons of cortex TNF-α; (c) Group comparisons of cortex TNFR1, TNF-α = Tumor necrosis factor-α, TNFR1 = Tumor necrosis factor receptor 1
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In the group comparisons of cortex TNF-α, MI + UCMS increased the concentration of cortex TNF-α significantly compared with sham and MI groups. While ABL pills attenuated the cortex inflammatory response by decreasing the cortex TNF-α [Figure 5]b. We could find the variation trend of cortex TNFR1 in the group comparisons, MI + UCMS group had a higher level of cortex TNFR1 compared with sham and MI, while ABL pills reversed the elevation, though without statistical significance (P > 0.05) [Figure 5]c.
Therefore, it was considered that the ABL pills could attenuate depressive behaviors via reducing cortex TNF-α/TNFR1.
| Discussion | | |
This study presents that ligation of LAD induces cardiac dysfunction and pathological changes accompanied by increasing cardiac TNF-α/TNFR1, and MI + UCMS induces depressive behaviors via increasing cortex TNF-α/TNFR1. While cardiac dysfunction and depressive behaviors could be reversed by anti-inflammation.
The main pathophysiological mechanism of MI involves inflammatory response.[22],[23]
Several main signaling pathways participate in the inflammation of MI, such as nucleotide-binding domain-like receptor protein 3 (NLRP3)/caspase-1, TLR4/MyD88/NF-κB, MAPK, and Wnt/β-catenin.[24] A high level of inflammatory cytokines could worsen adverse cardiac remodeling and link with increased mortality and morbidity of MI.[3] TNF-α is a key pro-inflammatory cytokine that was discovered in 1975.[25] Inflammation is a crucial initiator of MI. According to a clinical study, the elevation of TNF-α level indicates an increase of MI risk.[26] Therefore, in this study, the significant elevation of TNF-α presents the severe inflammation response in the heart post-MI. While binding to its receptor TNFR1, TNF-α actives the canonical NF-κB pathway and then contributes to cardiomyocyte death.[27] While attenuating inflammation could improve cardiac dysfunction and fibrosis, and reduce major adverse cardiac events.[28] Our study shows that the LV enlargement, and myocardial fibrosis formation in MI and MI + UCMS mice, are reversed by inflammation suppression [Figure 3]b.
The SPT is a classical method to evaluate the depressive behaviors of animals, which is widely used and acknowledged. The reduction of sucrose preference indicates anhedonia of animals, which is regarded as a crucial symptom of depression.[29] It has been used since 1987 by Willner et al.[30] Willner et al. proved that after exposure to chronic unpredictable mild stress, the sucrose preference of rats reduced, while the tricyclic antidepressant could reverse the reduction. Since then, a large number of experiments have applied SPT for measuring depressive behaviors. Therefore, we chose SPT for evaluating depressive behavior.
In this study, we discover that the depressive behaviors of the MI mice are associated with the elevation of cortex TNF-α. As far as we know, MI and UCMS induce cardiac and vascular inflammatory responses, and myocyte necrosis leads the cardiac myocytes and neurons to release TNF-α.[31] TNF-α could increase the permeability of the blood–brain barrier, and aggravate central nerve inflammation.[32] Hence, cortex inflammation initiates depressive behaviors, as we indicate in the study.
CD4 + Th cell subsets are critical players in tissue inflammation and autoimmunity.[33] Recently, Th cells are discovered to contribute to depression.[34] However, protective T cell autoimmunity could protect the heart from AMI injury.[35] Therefore, we study spleen Th1, Th2, and Treg by flow cytometry to further explore the immune-inflammation mechanism. However, our study did not find any apparent differences in spleen Th1, Th2, and Treg. Hence, we could not prove the specific effect of Th cell subsets in this experiment.
Both clinical and animal experimental studies report that natural medicine could benefit both MI and depression via anti-inflammatory effects.[6] This study reveals that ABL pills could improve cardiac function and depressive behaviors via inhibiting inflammation. Huang et al. discovered that ABL pills could protect the H9c2 cells from hypoxia/reoxygenation (HR) injury via the antioxidant effect and improving mitochondrial energy metabolism.[36] The anti-inflammation effect of ABL pills is closely related to its compositions. As a kind of Mongolian natural medicine, ABL pills include six kinds of herbs, involving Bos taurus domesticus Gmelin, Aucklandia lappa Decne, Choeros podias axillaris (Roxb), Eugenia caryophyllata Thunb, Liquidambar formosana Hance, Myristica fragrans Houtt. By applying the high-performance liquid chromatography-tandem quadrupole time-of-flight mass spectrometry (MS/MS) technology, the 119 kinds of chemical constitutions were identified, involving 36 organic acids, 22 flavonoids and their glycosides, 8 lignans, 3 sesquiterpene lactones, 6 terpenes, 3 coumarins, 17 phenols, 14 amino acids, 4 aldehydes, and 6 others.[37]
The three dominant components of Aucklandia lappa Decne are costunolide, dehydrocostuslactone, and alantolactone.[38],[39] Aucklandia lappa Decne could reduce the expression of IL-6, IL-1β, and TNF-α via NF-κB and MAPK signaling pathways, and depress oxidative response via Nrf2/HO-1 signaling pathway.[40] Choerospondias axillaris (Roxb) consist of alcohols, alkenes, aromatics, aldehydes and ketones, and esters.[41] The circulating ketones could benefit the treatment of heart failure via reducing cardiac NLRP3-inflammasome activation.[42] Liquidambar formosana Hance composes several main components such as flavonoids, triterpenoids, and tannins.[43] Triterpenoids, such as impressic acid and acankoreanogenin A, exert the anti-inflammation effect by reducing iNOS, COX-2, TNF-α, and IL-1β and suppressing the NF-κB signaling pathway.[44]
Limitation
In this study, the inflammatory response was presented by the variations of TNF-α and TNFR1 in cardiac and cortex tissues. We did not explore other cytokines and the related signaling pathways. Therefore, we could not better reveal the potential inflammation mechanisms of MI and depressive behaviors. In addition, 5-HT system dysfunction is regarded as a vital pathophysiological mechanism. However, there was a lack of further exploring the association between inflammation and 5-HT.
| Conclusions | | |
Inhibiting inflammation is effective in improving cardiac function and depressive behaviors. It will be promising in clinical practice in treating MI and depression post-MI.
Data availability
Data and materials have been provided in the sections of methods and results.
Authors' contributions
Meiyan Liu designed and supervised the experiment and revised the paper. Lijun Zhang conducted the data analysis and wrote the manuscript. Shuhui Tao, Nan Lu, Ruoyu Pan performed the experiment.
Financial support and sponsorship
This study was supported by National Natural Science Foundation of China (No. 81970447) and China Women's Development Foundation (2021573).
Conflicts of interest
Prof. Meiyan Liu is the Executive Editor-in-Chief of the Heart and Mind journal. The article was subject to the journal's standard procedures, with peer review handled independently of Prof. Meiyan Liu and their research groups. There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1]
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