The protective effect of misoprostol against doxorubicin induced liver injury

Bilğiç, Sedat; Özgöçmen, Meltem

doi:10.1080/10520295.2019.1605457

Cited by 21 publications

(19 citation statements)

References 34 publications

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“…Thus, similar to many chemotherapeutics like vincristine and cisplatin, in cancer cells, DOX intercalates with DNA strands and inhibits the activity of topoisomerase II enzyme and finally causes DNA double-strand breaks (Denard et al, 2011;Patel & Kaufmann, 2012). Among the many side effects of DOX, liver damage is one of the most common negative effects observed in use of this chemotherapeutic (Cainelli & Vallone, 2009;Hozayen et al, 2014).Many experimental studies have reported that DOX chemotherapy causes a serious hepatotoxicity (Bilgic & Ozgocmen, 2019;…”

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Therapeutic effects of thymoquinone in doxorubicin‐induced hepatotoxicity via oxidative stress, inflammation and apoptosis

Akın

Öztürk

Kaymak

et al. 2021

Anat Histol Embryol

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Chemotherapeutics are widely used in treatment of many cancer types. Despite antitumoural effects of these drugs in controlling the primary tumours and metastasis, they can cause a serious toxicity in healthy tissues due to their side effects and can worsen life quality of patients' (Martinel Lamas et al., 2015). Doxorubicin (DOX) is an anthracycline antibiotic which is widely used as a first chemotherapy treatment against several types of cancer. Thus, similar to many chemotherapeutics like vincristine and cisplatin, in cancer cells, DOX intercalates with DNA strands and inhibits the activity of topoisomerase II enzyme and finally causes DNA double-strand breaks (Denard et al., 2011;Patel & Kaufmann, 2012). Among the many side effects of DOX, liver damage is one of the most common negative effects observed in use of this chemotherapeutic (Cainelli & Vallone, 2009;Hozayen et al., 2014).Many experimental studies have reported that DOX chemotherapy causes a serious hepatotoxicity (Bilgic & Ozgocmen, 2019;

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confidence: 99%

“…Many experimental studies have reported that DOX chemotherapy causes a serious hepatotoxicity (Bilgic & Ozgocmen, 2019;…”

mentioning

confidence: 99%

Therapeutic effects of thymoquinone in doxorubicin‐induced hepatotoxicity via oxidative stress, inflammation and apoptosis

Akın

Öztürk

Kaymak

et al. 2021

Anat Histol Embryol

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“…Many experimental studies have reported that ADR chemotherapy causes serious hepatotoxicity by inducing the excessive formation of ROS and the overexpression of the genes involved in inflammatory pathways, and so inhibiting the antioxidant defense system and driving cell to apoptosis (9,13). In this experimental study, we observed that ADR administrations caused significant damage in the liver tissue including hemorrhage, necrotic hepatocytes, vacuolized hepatocytes, and irregular hepatocyte cords when compared to Control and CLQ groups.…”

Section: Discussion Discussionmentioning

confidence: 54%

“…Many experimental studies have reported that ADR chemotherapy causes serious hepatotoxicity (9,13). The mechanism of ADR toxicity has been associated with the oxidative stress state associated with the formation of an excessive amount of reactive oxygen species (ROS) and/or a reduction in the antioxidant defense system that causes unbalanced normal oxygen metabolism.…”

Section: Introduction Introductionmentioning

confidence: 99%

Investigation of the Therapeutic Effects of Chloroquine in Adriamycin-Induced Hepatotoxicity

Akın

Kaymak

Öztürk

et al. 2021

The EuroBiotech Journal

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The aim of this study is to investigate the therapeutic effects of Chloroquine (CLQ) against Adriamycin (ADR) induced hepatotoxicity. ADR is a chemotherapeutic agent used in the treatment of many cancer types, but it causes hepatotoxicity. CLQ is used as an anti-inflammatory drug in the treatment of malaria, rheumatoid arthritis, and pneumonia caused by Covid-19. Rats were divided into four groups: Control group, ADR group (2 mg/kg Adriamycin, one in three days for 30 days, i.p.), CLQ group (50 mg/kg Chloroquine, per day for 30 days, i.p.), ADR+CLQ (2 mg/kg Adriamycin, one in three days for 30 days, i.p. and 50 mg/ kg Chloroquine, per day for 30 days, i.p.). Animals were sacrificed, and liver tissues were extracted for further examinations. Histopathological changes in liver tissues were scored and IL-17 immunostaining was performed to determine the expression levels among experimental groups. Bodyweights in the ADR group decreased significantly compared to the Control group and CLQ group. Furthermore, bodyweight in ADR+CLQ group was significantly higher compared to ADR group. The histopathological score was significantly higher in ADR group when compared to Control and CLQ group while CLQ administrations reduced the damage induced by ADR in the ADR+CLQ group. IL-17 immunoreactivity was considerably increased in the ADR group. On the other hand, IL-17 expressions of ADR+CLQ were substantially less compared to ADR group. We suggest that CLQ can be used as a therapeutic agent to reduce the detrimental effects of ADR, thanks to its anti-inflammatory properties.

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“…Мієлосупресія, стоматит, ураження шлунково-кишкового тракту, алопеція є його найбільш частими оборотними токсичними ефектами [24]. У клінічних і експериментальних дослідженнях доведені такі побічні ефекти доксорубіцину, як кардіотоксичність, нефротоксичність, гепатотоксичність [8,10,12,14,16,20,[22][23][24].…”

Section: вступunclassified

S-Ademethionine Effect on Pathogenetic Mechanisms of Doxorubicin-Induced Liver Injury in Rats With Non-Alcoholic Steatohepatitis

Маслова¹,

Skrypnyk²

2020

Clin. and experim. pathol.

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Українська медична стоматологічна академія, м. Полтава Мета роботи-дослідити вплив S-адеметіоніну на зміни прооксидантноантиоксидантного статусу та аргінін/цитрулінового циклу на фоні доксорубіциніндукованого ураження печінки у щурів із неалкогольним стеатогепатитом. Матеріали і методи. Дослідження проведені на 30 білих нелінійних статевозрілих щурах, із них 15 (50%) самців, 15 (50%)-самок, масою 160-220 г. Щурів розподіляли на 3 групи: І (n=10)-щури (5 самців і 5 самок), яким із 1-го по 63-й день моделювали неалкогольний стеатогепатит (НАСГ), потім упродовж 3-х днів (з 64-го по 66-й) внутрішньочеревно вводили доксорубіцин із розрахунку 5 мг/кг/добу із досягненням кумулятивної дози 15 мг/кг і 0,9% розчин натрію хлориду внутрішньочеревно 1 мл; ІІ (n=10)-щури (5 самців і 5 самок), яким моделювали НАСГ і вводили доксорубіцин аналогічно І групі і S-адеметіонін (SАМе)внутрішньочеревно 100 мг/кг/добу із сумарною дозою 300 мг/кг; ІІІ (n=10)-щури (5 самців і 5 самок), які склали групу контролю. У гомогенаті печінки визначали вміст ТБК-реактантів, аргініну, цитруліну, активність каталази, аргінази, орнітиндекарбоксилази (ОДК). Результати. На фоні введення доксорубіцину у щурів із НАСГ спостерігалося зростання вмісту ТБК-реактантів при одночасному зниженні активності каталази, що супроводжувалося зменшенням активності аргінази і ОДК порівняно з контролем (р<0,05). Введення SАМе дало змогу зменшити прояви оксидативного стресу, потенційованого доксорубіцином, а також запобігти порушенню детоксикаційної і білковосинтезувальної функції печінки. Висновки. У щурів із НАСГ введення SАМе зменшує прояви оксидативного стресу, потенційованого доксорубіцином, та запобігає порушенням детоксикаційної і білковосинтезувальної функцій печінки, що виникають під впливом цього препарату.

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The protective effect of misoprostol against doxorubicin induced liver injury

Cited by 21 publications

References 34 publications

Therapeutic effects of thymoquinone in doxorubicin‐induced hepatotoxicity via oxidative stress, inflammation and apoptosis

Therapeutic effects of thymoquinone in doxorubicin‐induced hepatotoxicity via oxidative stress, inflammation and apoptosis

Investigation of the Therapeutic Effects of Chloroquine in Adriamycin-Induced Hepatotoxicity

S-Ademethionine Effect on Pathogenetic Mechanisms of Doxorubicin-Induced Liver Injury in Rats With Non-Alcoholic Steatohepatitis

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