Aloin protects against arsenic trioxide–induced myocardial membrane damage and release of inflammatory cytokines

Birari, Lalit A; Mahajan, Umesh B; Patil, Kiran; Patil, Dipak D.; Bagul, Neha A; Belemkar, Sateesh; Goyal, Sameer N.; Ojha, Shreesh; Patil, Chandragouda R.

doi:10.1007/s00210-020-01833-1

Cited by 18 publications

(14 citation statements)

References 17 publications

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“…For the estimation of activity of superoxide dismutase (SOD)/catalase and reduced glutathione (GSH), 10% tissue homogenate was prepared in PBS and for the determination of lipid peroxidation (MDA level), the tissue homogenate was prepared in KCl solution [7].…”

Section: Estimation Of Oxidative Stress Parametersmentioning

confidence: 99%

“…At higher concentrations, free radical-scavenging activity of aloin, relatively outweighs its reducing power and thereby protects the DNA [6]. However, this duality of aloin effects observed in the in vitro experiments is not replicated in the in vivo experimental studies [7]. Doxorubicin (DOX), an anthracycline anticancer agent, is used in the treatment of a variety of cancers including breast, bladder, stomach, lung, and ovarian cancer.…”

Section: Introductionmentioning

confidence: 99%

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Aloin alleviates doxorubicin-induced cardiotoxicity in rats by abrogating oxidative stress and pro-inflammatory cytokines

Birari

Wagh

Patil

et al. 2020

Cancer Chemother Pharmacol

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Purpose Aloin, an anthraquinone present in the aloe species, possesses antiangiogenic, chemopreventive and antioxidant properties. It exerts cytotoxicity against breast cancer and ovarian cancer cell lines. These properties of aloin project it as a chemopreventive adjuvant to anticancer chemotherapy. Methods We evaluated the effect of concurrent oral administration of aloin against doxorubicin (DOX)-induced cardiotoxicity in rats. The protective effects of aloin against DOX-induced toxicity were evident as a statistically significant inhibition of a rise in the biochemical markers of myocardial damage including lactate dehydrogenase (LDH), creatinine kinasemyocardial band (CK-MB), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Results Aloin dose dependently inhibited the DOX-induced changes in ECG like increased ST-height and prolonged QT interval. It protected heart against the lipid peroxidation and restored the levels of antioxidative defenses: reduced glutathione, catalase and superoxide dismutase. Aloin prominently reduced the levels of proinflammatory cytokines-TNF-α, IL-1β and IL-6. Notably, the significant protective effects of aloin were evident even at the strikingly lower doses of 1 and 5 mg/kg per day. Conclusion Our results highlight the necessity to further investigate the chemopreventive effects of aloin against other chemotherapeutic agents.

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Section: Estimation Of Oxidative Stress Parametersmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Aloin alleviates doxorubicin-induced cardiotoxicity in rats by abrogating oxidative stress and pro-inflammatory cytokines

Birari

Wagh

Patil

et al. 2020

Cancer Chemother Pharmacol

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“…Recent studies have demonstrated that oxidative stress injury, inflammation and apoptosis of myocardial cells are potential mechanisms associated with ATO-induced cardiotoxicity, in which oxidative stress is the main cause (Chang et al, 2007;Das et al, 2010;Ye et al, 2010;Birari et al, 2020;Xue et al, 2020). Reactive oxygen species (ROS) are produced through a series of extracellular and intracellular activities, considered as a novel signalling mediator involved in cell growth, differentiation, progression and death (Sena and Chandel, 2012;Zhang et al, 2013a).…”

Section: Introductionmentioning

confidence: 99%

Based on Activation of p62-Keap1-Nrf2 Pathway, Hesperidin Protects Arsenic-Trioxide-Induced Cardiotoxicity in Mice

Jia

et al. 2021

Front. Pharmacol.

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Background: Hesperidin (HES) is a flavonoid glycoside found in the tangerine peel and has antioxidant properties. Arsenic trioxide (ATO) is an anti-tumour drug; however, its serious cardiotoxicity limits its clinical application. In addition, the protection of HES against ATO-induced cardiotoxicity has not been explored.Objective: The study aims to investigate and identify the underlying effect and mechanism of HES on ATO-induced cardiotoxicity.Methods: Fifty mice were randomly assigned to five groups. Mice were orally given HES:100 or 300 mg/kg/day concurrently and given ATO intraperitoneal injections: 7.5 mg/kg/day for 1 week. Blood and heart tissues were collected for examination. Evaluated in serum was the levels of creatine kinase (CK), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI). In addition, evaluated in heart tissues were the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), catalase (CAT), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, cleaved-Caspase-3, p62, Kelch-like ECH-associated protein 1 (Keap1), and nuclear factor erythroid 2-related factor 2 (Nrf2). The heart tissues were also examined for histopathology and mitochondrial ultrastructure.Results: Compared with the ATO group, the HES treatment groups reduced the levels of CK, LDH, cTnI, ROS, MDA, TNF-α, IL-6, Bax, Caspase-3, cleaved-Caspase-3 and Keap1 and enhanced the levels of SOD, GSH, CAT, Bcl-2, p62 and Nrf2.Conclusions: The results demonstrate that HES protects against ATO-induced cardiotoxicity, through inhibiting oxidative stress, and subsequent inflammation and apoptosis. The underlying results are closely related to the regulation of the p62-Keap1-Nrf2 signalling pathway.

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“…It has been demonstrated that aloin is effective in reducing the production of inflammatory and proinflammatory factors [ 37 , 38 ]. A previous study reported that aloin treatment significantly decreased the expression of iNOS and TNF- α [ 48 ], while other studies found that aloin exerted anti-inflammatory activity and reduced the release of inflammatory cytokines [ 49 , 50 ]. Correspondingly, we demonstrated the protective effects of aloin on TNF- α -treated NPCs.…”

Section: Discussionmentioning

confidence: 99%

Aloin Regulates Matrix Metabolism and Apoptosis in Human Nucleus Pulposus Cells via the TAK1/NF-κB/NLRP3 Signaling Pathway

Chen

Qiu

et al. 2022

Stem Cells International

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Intervertebral disc degeneration (IDD) is a degenerative disease that is characterized by decreased matrix synthesis and extra degradation, nucleus pulposus cells (NPCs) apoptosis, and infiltration of inflammatory factors. Aloin, a colored compound from aloe plants, has been shown to be effective against skeletal degenerative diseases, but it is unclear whether it is protective against IDD. Herein, we investigated the role of aloin in NPCs. In our study, the upregulation of proinflammatory factors, apoptosis, and unbalanced matrix metabolism were observed in degenerative NP tissues. We found that aloin had a curative effect on extracellular matrix metabolism and apoptosis in TNF-alpha- (TNF-α-) treated NPCs by inhibiting oxidative stress and the proinflammatory factor expression. Further investigation revealed that aloin treatment suppressed the TAK1/NF-κB pathway. Moreover, the expression level of the NLPR3 inflammasome was downregulated after aloin treatment in TNF-α-treated NPCs. In summary, our results demonstrated that aloin treatment can reverse TNF-α-induced unbalanced matrix metabolism and apoptosis of NPCs via the TAK1/NF-κB/NLRP3 axis. This study supports that aloin can be a promising therapeutic agent for IDD.

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Aloin protects against arsenic trioxide–induced myocardial membrane damage and release of inflammatory cytokines

Cited by 18 publications

References 17 publications

Aloin alleviates doxorubicin-induced cardiotoxicity in rats by abrogating oxidative stress and pro-inflammatory cytokines

Aloin alleviates doxorubicin-induced cardiotoxicity in rats by abrogating oxidative stress and pro-inflammatory cytokines

Based on Activation of p62-Keap1-Nrf2 Pathway, Hesperidin Protects Arsenic-Trioxide-Induced Cardiotoxicity in Mice

Aloin Regulates Matrix Metabolism and Apoptosis in Human Nucleus Pulposus Cells via the TAK1/NF-κB/NLRP3 Signaling Pathway

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