Attenuation effect of Abnormal Savda Munziq on liver and heart toxicity caused by chemotherapy in mice

Aikemu, Ainiwaer; Amat, Nurmuhamat; Yusup, Abdiryim; Shan, Lianlian; Qi, Xinwei; Upur, Halmurat

doi:10.3892/etm.2016.3328

Cited by 19 publications

(15 citation statements)

References 50 publications

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“…First, it was previously demonstrated that a similar 5‐FU protocol was not associated with any cellular or functional cardiotoxic effects . Second, the frequency and duration of 5‐FU treatment in the present study were different from other studies reporting the cardiotoxicity of this agent . Third, there was no elevation of ANP or BNP expression in control or swum mice receiving 5‐FU.…”

Section: Discussioncontrasting

confidence: 81%

Cardiac cell proliferation is not necessary for exercise‐induced cardiac growth but required for its protection against ischaemia/reperfusion injury

Bei

Chen

et al. 2017

J Cellular Molecular Medi

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The adult heart retains a limited ability to regenerate in response to injury. Although exercise can reduce cardiac ischaemia/reperfusion (I/R) injury, the relative contribution of cardiac cell proliferation including newly formed cardiomyocytes remains unclear. A 4-week swimming murine model was utilized to induce cardiac physiological growth. Simultaneously, the antineoplastic agent 5-fluorouracil (5-FU), which acts during the S phase of the cell cycle, was given to mice via intraperitoneal injections. Using EdU and Ki-67 immunolabelling, we showed that exerciseinduced cardiac cell proliferation was blunted by 5-FU. In addition, the growth of heart in size and weight upon exercise was unaltered, probably due to the fact that exercise-induced cardiomyocyte hypertrophy was not influenced by 5-FU as demonstrated by wheat germ agglutinin staining. Meanwhile, the markers for pathological hypertrophy, including ANP and BNP, were not changed by either exercise or 5-FU, indicating that physiological growth still developed in the presence of 5-FU. Furthermore, we showed that CITED4, a key regulator for cardiomyocyte proliferation, was blocked by 5-FU. Meanwhile, C/EBPb, a transcription factor responsible for both cellular proliferation and hypertrophy, was not altered by treatment with 5-FU. Importantly, the effects of exercise in reducing cardiac I/R injury could be abolished when cardiac cell proliferation was attenuated in mice treated with 5-FU. In conclusion, cardiac cell proliferation is not necessary for exercise-induced cardiac physiological growth, but it is required for exercise-associated protection against I/R injury.

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Section: Discussioncontrasting

confidence: 81%

Cardiac cell proliferation is not necessary for exercise‐induced cardiac growth but required for its protection against ischaemia/reperfusion injury

Bei

Chen

et al. 2017

J Cellular Molecular Medi

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“…On the other hand, luteolin prevented the reduction in spleen and liver weights induced by irinotecan. Chemotherapy toxicity in organs not affected by cancer is one of its limitations (Aikemu et al, ), and the hepatotoxic side effects have been a serious clinical challenge in chemotherapy (Thatishetty, Agresti, & O'Brien, ). In our experiments, irinotecan increases the plasma levels of AST and ALT, whereas luteolin treatment prevented the increase in ALT, findings similar to those of other authors evaluating hepatoprotective effects of this compound (Liu et al, ; He et al, ).…”

Section: Discussionmentioning

confidence: 99%

Luteolin prevents irinotecan‐induced intestinal mucositis in mice through antioxidant and anti‐inflammatory properties

Boeing

Souza

Speca

et al. 2020

British J Pharmacology

103

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Background and Purpose: Intestinal mucositis refers to mucosal damage caused by cancer treatment, and irinotecan is one of the agents most associated with this condition. Focusing on the development of alternatives to prevent this important adverse effect, we evaluated the activity of the flavonoid luteolin, which has never been tested for this purpose despite its biological potential. Experimental Approach: The effects of luteolin were examined on irinotecaninduced intestinal mucositis in mice. Clinical signs were evaluated. Moreover, histological, oxidative, and inflammatory parameters were analysed, as well as the possible interference of luteolin in the anti-tumour activity of irinotecan. Key Results: Luteolin (30 mgÁkg −1 ; p.o. or i.p.) prevented irinotecan-induced intestinal damage by reducing weight loss and diarrhoea score and attenuating the shortening of the duodenum and colon. Histological analysis confirmed that luteolin (p.o.)prevented villous shortening, vacuolization, and apoptosis of cells and preserved mucin production in the duodenum and colon. Moreover, luteolin treatment mitigated irinotecan-induced oxidative stress, by reducing the levels of ROS and LOOH and augmenting endogenous antioxidants, and inflammation by decreasing MPO enzymic activity, TNF, IL-1β, and IL-6 levels and increasing IL-4 and IL-10. Disruption of the tight junctions ZO-1 and occludin was also prevented by luteolin treatment.Importantly, luteolin did not interfere with the anti-tumour activity of irinotecan. Conclusion and Implications: Luteolin prevents intestinal mucositis induced byirinotecan and therefore could be a potential adjunct in anti-tumour therapy to control this adverse effect, increasing treatment adherence and consequently the chances of cancer remission.

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“…Thus, their prolonged use and over dosage cause death. These drugs cause disruption in basal metabolism by showing toxic effect especially in liver and hearth tissues [16]. The biochemical and electron microscopic findings showed that DO x causes he patotoxic effect.…”

Section: Doxorubicin-induced Hepatotoxicitymentioning

confidence: 99%

“…DO x has showed cardiotoxic and hepatotoxic effects in animals. It is known that DOX cause weight loss [13,16]. Thus, their prolonged use and over dosage cause death.…”

Section: Doxorubicin-induced Hepatotoxicitymentioning

confidence: 99%

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Reduction of Hepatotoxicity Induced by Doxorubicin

Bengaied¹,

Ribeiro²,

Amri³

et al. 2017

J Integr Oncol

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Doxorubicin (DOX) has been used in the treatment of variety of cancers but its administration is limited by a dosedependent toxicity. Its cytotoxic effects on malignant cells have shown an increase in the risk of cardiotoxicity, hepatoxicity, renal insufisance.Antioxydants have been explored for both their cancer preventive properties and chemodulatory of DOX toxicity. Resveratrol (RSV) is a polyphenolic constituent of several dietary mainly of grapes and wine origin recently its anticancer potential has been extensively explored, revealing its anti-proliferative effect on different cancer cell lines, both in vitro and in vivo. RSV is also known to have modulatory effects on cell apoptosis, migration and growth via various signaling pathways. Though, RSV possesses great medicinal value, its applications as a therapeutic drug is limited. Problems like low oral bioavailability and poor aqueous solubility make RSV an unreliable candidate for therapeutic purposes. Additionally, the rapid gastrointestinal digestion of RSV is also a major barrier for its clinical translation. Hence, to overcome these disadvantages RSV-based nanodelivery systems have been considered in recent times. Nanodelivery systems of RSV have shown promising results in its uptake by the epithelial system as well as enhanced delivery to the target site. Herein we have tried to bring new new insights into the molecular mechanisms of DOX toxicity with respect to DNA damage, free radicals and whether RSV can be a playmaker as chemodulatory of DO x .

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Attenuation effect of Abnormal Savda Munziq on liver and heart toxicity caused by chemotherapy in mice

Cited by 19 publications

References 50 publications

Cardiac cell proliferation is not necessary for exercise‐induced cardiac growth but required for its protection against ischaemia/reperfusion injury

Cardiac cell proliferation is not necessary for exercise‐induced cardiac growth but required for its protection against ischaemia/reperfusion injury

Luteolin prevents irinotecan‐induced intestinal mucositis in mice through antioxidant and anti‐inflammatory properties

Reduction of Hepatotoxicity Induced by Doxorubicin

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