Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction

Ma, Lina; Lian-da, LI; Li, Shao-chun; Hao, Xin-mei; Zhang, Jinyan; He, Ping; Li, Yikui

doi:10.1007/s11655-016-2523-0

Cited by 25 publications

(22 citation statements)

References 37 publications

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“…Allicin is isolated from garlic and may also be extracted as a brownish orange dry resin from the Garcinia hanburyi tree occurring in South-East Asia (11,12). In previous years, Asians have used allicin as a traditional medicine for the therapy of various diseases.…”

Section: Introductionmentioning

confidence: 99%

Allicin activates autophagic cell death to alleviate the malignant development of thyroid cancer

Xiang

Zhao

et al. 2018

Exp Ther Med

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Abstract. Allicin has been reported to inhibit cancer cell proliferation, induce cell apoptosis and enhance the accumulation of reactive oxygen species. However, it has remained elusive whether allicin improves multidrug resistance in thyroid cancer cells through modulating autophagy. The present study demonstrated that combined use of allicin and cisplatin or carboplatin resulted in an enhanced growth inhibitory effect on SW1736 and HTh-7 cells. Furthermore, treatment with allicin significantly increased SW1736 and HTh-7 cell autophagy. Of note, allicin-induced cell death was largely abolished by 3-methyladenine or chloroquine treatment, suggesting that allicin-induced A549 cell death was dependent on autophagy. Western blot analysis demonstrated that allicin treatment inhibited the activation of Akt, mammalian target of rapamycin and S6. Furthermore, it was demonstrated that combined use of allicin and rapamycin induced more cell death compared with that induced by allicin or rapamycin alone. In conclusion, allicin may serve as an adjunctive therapy for thyroid cancer, as it induces autophagy-dependent cell death even when cancer cells have developed apoptosis resistance.

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Section: Introductionmentioning

confidence: 99%

Allicin activates autophagic cell death to alleviate the malignant development of thyroid cancer

Xiang

Zhao

et al. 2018

Exp Ther Med

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“…Allicin has been shown to exert a wide range of biological effects, including antioxidant activity, the inhibition of platelet activation, antitumor activity, and antimicrobial activity [ 9 – 12 ]. Our previous studies in rats found that allicin mitigates ischemic injury via inhibiting apoptosis [ 13 ]. It was also shown to prevent against myocardial apoptosis and fibrosis in a streptozotocin-induced diabetic models in rats [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of Allicin against Ischemia/Hypoxia‐Induced H9c2 Myoblast Apoptosis via eNOS/NO Pathway‐Mediated Antioxidant Activity

Chen²,

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Allicin (2-propene-1-sulfinothioic acid S-2-propenyl ester, diallyl thiosulfinate) is the main biologically active ingredient in garlic. The present study investigated the protective effect of allicin against cardiomyocyte apoptosis that was induced by ischemia in vitro and the potential molecular mechanisms that were involved in this antiapoptotic effect. The results indicated that allicin increased H9c2 cell activity and attenuated the rate of apoptosis that was induced by ischemia/hypoxia. Intracellular calcium concentrations significantly decreased in the allicin-treated groups. Bax expression significantly decreased, and Bcl-2 expression increased in allicin-treated rats. Nitric oxide blockade significantly inhibited these effects. Allicin also increased the activity of SOD and NO release and decreased MDA levels. Allicin significantly increased the expression of eNOS, Nrf2, and HO-1 proteins. Collectively, these findings demonstrate that allicin protects H9c2 cells against apoptosis, and this protective effect appears to occur via eNOS/NO pathway-mediated antioxidant activity.

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“…Apoptosis is an important physiological process that supports biological life and normal activities (23). If the signal transmission pathways that control and regulate apoptosis are severely disrupted, this causes a number of human diseases, including cancer and infectious diseases (24).…”

Section: Discussionmentioning

confidence: 99%

miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression

Sun

Cai

et al. 2018

Mol Med Report

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The aim of the present study was to evaluate the functional association between the expression of miR‑483‑3p and acute myocardial infarction (AMI) in patients and in vitro. H9c2 cells were incubated in a vacuum with 5% CO2, 5% H2 and 90% N2 for 2 h, which generated the AMI model in vitro. Reverse transcription‑quantitative polymerase chain reaction was used to measure miR‑483‑3p expression, and flow cytometry analysis and ELISA analysis were used to analyze apoptosis rate via caspase‑3 and caspase‑9 activity kits. B‑cell lymphoma 2 (Bcl‑2)/Bcl‑2‑associated X protein (Bax) and transcriptionally suppressed the protein expression of insulin growth factor 1 (IGF‑1) were analyze using western blot analysis. The results demonstrated that the expression of miR‑483‑3p in patients with AMI was increased when compared with the control group. In the in vitro model, the overexpression of miR‑483‑3p promoted apoptosis, increased caspase‑3 and caspase‑9 activity levels, induced the protein expression of Bcl‑2/Bax and IGF‑1. Picropodophyllotoxin, an IGF‑1 inhibitor, was administered to cells following the overexpression of miR‑483‑3p. Administration of picropodophyllotoxin suppressed IGF‑1 protein expression, promoted apoptosis, increased caspase‑3 and caspase‑9 activity levels, and induced the protein expression of Bax/Bcl‑2. The results of the present study revealed that miR‑483‑3p may regulate AMI via the IGF‑1 signaling pathway and may support the restoration of functional performance following AMI.

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Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction

Abstract: Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis, further improving cardiac function.

Cited by 25 publications

References 37 publications

Allicin activates autophagic cell death to alleviate the malignant development of thyroid cancer

Allicin activates autophagic cell death to alleviate the malignant development of thyroid cancer

Effect of Allicin against Ischemia/Hypoxia‐Induced H9c2 Myoblast Apoptosis via eNOS/NO Pathway‐Mediated Antioxidant Activity

miR-483-3p regulates acute myocardial infarction by transcriptionally repressing insulin growth factor 1 expression

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