Fargesin as a potential β1 adrenergic receptor antagonist protects the hearts against ischemia/reperfusion injury in rats via attenuating oxidative stress and apoptosis

Wang, Xin; Cheng, Yongjie; Xue, Hui; Yue, Yuan; Zhang, Weifang; Li, Xiaoni

doi:10.1016/j.fitote.2015.05.016

Cited by 22 publications

(12 citation statements)

References 49 publications

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“…Some previous studies have shown that cAMP/PKA could protect livers from I/R injury [18,34]. The cAMP/PKA pathway was also proven to play a role against myocardial I/R injury in mice [35].…”

Section: Discussionmentioning

confidence: 96%

Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

Zhang

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNA (lncRNA) and glucagon-like peptide 1 receptor (GLP-1R) are crucial for heart development and for adult heart structural maintenance and function. Herein, we performed a study to explore the effect of lncRNA LINC00652 (LINC00652) on myocardial ischemia-reperfusion (I/R) injury by targeting GLP-1R through the cyclic adenosine monophosphate-protein kinase A (cAMP/PKA) pathway. Methods: Bioinformatics software was used to screen the long-chain non-coding RNAs associated with myocardial ischemia-reperfusion and to predict target genes. The mRNA and protein levels of LINC00652, GLP-1R and CREB were detected by RT-qPCR and western blotting. In order to identify the interaction between LINC00652 and myocardial I/R injury, the cardiac function, the hemodynamic changes, the pathological changes of the myocardial tissues, the myocardial infarct size, and the apoptosis of myocardial cells of mice were measured. Meanwhile, the levels of serum IL-1β and TNF-α were detected. Results: LINC00652 was overexpressed in the myocardial cells of mice with myocardial I/R injury. GLP-1R is the target gene of LINC00652. We also determined higher levels of LINC00652 and GLP-1R in the I/R modeled mice. Additionally, si-LINC00652 decreased cardiac pathology, infarct size, apoptosis rates of myocardial cells, and levels of IL-1β and TNF-α, and increased GLP-1R expression cardiac function, normal hemodynamic index, and the expression and phosphorylation of GLP-1R and CREB proteins. Conclusion: Taken together, our key findings of the present highlight LINC00652 inhibits the activation of the cAMP/PKA pathway by targeting GLP-1R to reduce the protective effect of sevoflurane on myocardial I/R injury in mice.

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Section: Discussionmentioning

confidence: 96%

Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

Zhang

Liu

et al. 2018

Cell Physiol Biochem

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“…The levels of reduced glutathione and the activities of glutathione peroxidase in the ISO-induced myocardial infarcted rats were significantly decreased, when compared to that in normal control rats. This decrease in GSH level in ISO-treated rat might be due to its increased utilization in protecting–SH group containing proteins from free radicals or due to enhanced protective mechanism to oxidative stress in myocardial injury 45 .…”

Section: Discussionmentioning

confidence: 95%

Preventive effect of Agnucastoside C against Isoproterenol-induced myocardial injury

Panda

Kar

Biswas

2017

Sci Rep

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An iridoid glycoside, agnucastoside C (ACC) was isolated from the leaves of Moringa oliefera and its cardio protective potential was investigated in adult rats by examining the effects of this test compound, ACC at 30 mg/kg for 14 days in isoproterenol (100 mg/kg)-induced myocardial injury. Isoproterenol (ISO) administration induced the myocardial injury as evidenced by the altered ECG pattern with ST-segment elevation and an increase in the levels of cardiac injury markers including troponin-I, creatine kinase-MB, alanine transaminase, aspartate transaminase, lactate dehydrogenase; inflammatory markers, interleukine-6 and tumor necrosis factor. In this group, there was also an increase in cardiac lipid peroxidation and a decrease in cellular antioxidants. However, pretreatment with ACC maintained the normal ECG pattern and nearly normal levels of all the cardiac markers in ISO-induced animals. Electron microscopic and histological studies also showed marked reduction in ISO-induced cardiac damages including infarct size by ACC. Analysis by 2-DE revealed the involvement of 19 different cardiac proteins, associated with energy metabolism, oxidative stress and maintenance of cytoskeleton. The expression of those proteins were altered by ISO, but maintained in ACC pretreated rats. Our findings reveal the potential of isolated ACC in the prevention of myocardial damage.

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“…A previous study reported that sesamin was a potent stimulator of melanogenesis in B16 cells [14], while another study showed that sesamin blocked melanin induction and melanogenic enzyme production [15]. Although the anti-inflammatory and antioxidant properties of fargesin have been elucidated [16,17], its function in depigmentation is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Fargesin inhibits melanin synthesis in murine malignant and immortalized melanocytes by regulating PKA/CREB and P38/MAPK signaling pathways

Chai

Shi

et al. 2019

Journal of Dermatological Science

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Background: Fargesin is commonly used in the treatment of allergic rhinitis, inflammation, sinusitis and headache. Objective: The aim of the study is to investigate a new function of fargesin against melanin production and its underlying molecular mechanism. Methods: B16F10 mouse melanoma cells, Melan-a and human epidermal melanocytes were treated with different concentrations of fargesin for the indicated time. The extracellular and cellular melanin content was detected by spectrometry at 490 nm and 405 nm, respectively. RT-qPCR and Western blot analysis were used to exam the expression of melanogenic enzymes and the activities of PKA/CREB and p38 MAPK pathway components. Zebrafish was used as an in vivo model for studying the function of fargesin in regulating melanogenesis. Results: Fargesin effectively inhibited melanin production at moderate dose in mouse B16F10 melanoma cells, normal melanocyte cell lines and zebrafish. The expression of microphthalmia-associated transcription factor (MITF), its downstream melanogenic enzymes and tyrosinase activity were also strongly reduced by fargesin. Moreover, the increase of melanin production induced by UVB and forskolin could be fully reversed by fargesin treatment. Fargesin also effectively inhibited the activation of PKA/ CREB and p38 MAPK as well as their interactions, which in turn is responsible for the expression of MITF and melanogenic enzymes. Conclusions: These results show that fargesin can function as an anti-melanogenic agent, at least in part, by inhibiting PKA/CREB and p38/MAPK signaling pathways. Therefore, fargesin and its derivatives may potentially be used for preventing hyperpigmentation disorders in the future.

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Fargesin as a potential β1 adrenergic receptor antagonist protects the hearts against ischemia/reperfusion injury in rats via attenuating oxidative stress and apoptosis

Cited by 22 publications

References 49 publications

Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

Preventive effect of Agnucastoside C against Isoproterenol-induced myocardial injury

Fargesin inhibits melanin synthesis in murine malignant and immortalized melanocytes by regulating PKA/CREB and P38/MAPK signaling pathways

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