Probing the biological evaluations of a new designed Pt(II) complex using spectroscopic and theoretical approaches: human hemoglobin as a target

Abazari, Omid; Shafaei, Zahra; Divsalar, Adeleh; Eslami-Moghadam, Mahbubeh; Ghalandari, Behafarid; Saboury, Ali Akbar

doi:10.1080/07391102.2015.1071280

Cited by 39 publications

(11 citation statements)

References 54 publications

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“…Recently, piperine’s potential cytotoxic and anti-tumorigenic properties in against several types of cancer cells have been reported ( 15 ). In recent years, numerous experiments in vitro and vivo have reported that the anti-tumor activity of piperine may partly be due to its effects on signaling pathways involved in apoptosis of cancer cells ( 15 – 18 ).…”

Section: Introductionmentioning

confidence: 99%

The Synergistic Combination of Cisplatin and Piperine Induces Apoptosis in MCF-7 Cell Line

Fattah¹,

Morovati²,

Niknam³

et al. 2021

ijph

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Background: Piperine is a natural compound obtained from the Piper nigrum that exhibits anti-proliferative and anti-cancer activity in cancer cell lines. We analyzed the cytotoxic effect of piperine combined with cisplatin compound in the human MCF-7 breast cancer cell line and the underlying mechanism. Methods: The present in vitro study was performed on MCF-7 cell line in Jahrom University of Medical Sciences between, Jahrom, Iran from 2016 to 2017. Cultured MCF-7 cells were seeded into four groups: a control group (untreated group), a group treated with cisplatin, a group treated with piperine and a group treated with cisplatin and piperine. Cell viability was analyzed using the MTT assay method. Flow c-ytometric analysis was investigated for apoptosis. The mRNA and protein expression of the apoptotic regulators p53, Bcl-2, Bax, caspase 3 and caspase 9 were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting analysis. Results: Piperine (20 and 30 µM) in combination with cisplatin (5, 10 and 15 µM) for 24 h synergistically inhibited cell viability of MCF-7 breast cancer cells more than piperine and cisplatin used alone. Synergistic antibreast cancer activities cisplatin (5 µM) and piperine (20 µM) were via inducing apoptosis. Piperine (20 µM) and cisplatin (5 µM) for 24 h induce apoptosis strongly through reduction of Bcl-2 and increase of caspase 3, p53, caspase 9, and Bax. Conclusion: Piperine in combination with cisplatin could trigger p53-mediated apoptosis more effective than cisplatin alone in MCF-7 breast cancer cells, reducing the toxic dose of cisplatin used in cancer chemotherapy.

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Section: Introductionmentioning

confidence: 99%

The Synergistic Combination of Cisplatin and Piperine Induces Apoptosis in MCF-7 Cell Line

Fattah¹,

Morovati²,

Niknam³

et al. 2021

ijph

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“…In the present study, the effect of silibinin was examined on the serum indicators of liver tissue injury, as well as Cx43, Cx32, and Cx26 gene expression during warm hepatic IR. The IRI frequently occurs during transplantation and hepatic surgery; moreover, it promotes molecular reactions that enhance damage in the liver parenchyma (22)(23)(24). Several studies reported that GJ proteins are involved in liver IRI (7,25).…”

Section: Discussionmentioning

confidence: 99%

Alteration of connexins gene expression by silibinin during hepatic warm ischemia-reperfusion injury in the rat model

Ghobadi

Mousavi

Mosavi

et al. 2021

ircmj

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Background: Ischemia-reperfusion injury (IRI) is an injurious phenomenon that is the primary determinant of liver dysfunction after surgery and transplantation. The present evidence demonstrated that connexin 43 (Cx43), Cx32, and Cx26 are the essential gap junction proteins involved in the liver IRI. This study aimed to characterize the beneficial effects of silibinin on Cx43, Cx32, and Cx26 gene expression during warm hepatic ischemia-reperfusion (IR). Materials and Methods: A total of 32 male Wistar rats weighing 250-300 g were randomly divided into four equal groups of eight animals in each group as follows: 1) control group (laparotomy+normal saline), 2) laparotomy+silibinin (30 mg/kg) (SILI), 3) liver IR procedure+normal saline (IR), and 4) liver IR procedure+silibinin (30 mg/kg) (IR+SILI). After 1 h of ischemia followed by 3 h of reperfusion, blood samples and tissue sections were gathered to assess the serum liver markers and evaluate the liver histological changes as well as gene expression, respectively. Results: The obtained data proved no considerable differences between control and SILI groups in all experiments. Furthermore, the gene expression of Cx26, Cx32, and Cx43 was significantly induced in the IR group, compared to the control group. Silibinin markedly reduced Cx26 and Cx32 mRNA expression, whereas increased Cx43 mRNA expression. Moreover, serum alanine aminotransferase and aspartate aminotransferase levels were markedly elevated in the IR group (P<0.001), compared to the control group. However, in the IR+SILI group, silibinin could significantly decline these elevations, compared to the IR group. In addition, silibinin diminished hepatic tissue damages during IR. Conclusion: Silibinin could attenuate liver injury through better cell-to-cell communication via lowering Cx32 and Cx26, as well as increasing Cx43 gene expression, respectively.

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“…Several reported works explain the interaction of the various compounds with Hb. Such as oxali‐palladium, [13] Pt(II) complex, [14] etc., anion exchange inhibitor, e. g., DIDS & antiseptic drug, e. g., DNP [5a] . Nevertheless, there are few reports which study the interaction between Hb and anticancer drug directly [7c,d] …”

Section: Introductionmentioning

confidence: 99%

Study of Anticancer Drugs Interaction with Hemoglobin by Electrochemical Methods and Molecular Docking: Implications towards Anticancer Treatment

2021

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Chemotherapeutic drugs tend to cause hemolysis; however, hemoglobin's mode of action is still less explored. In the present study, we used electrochemical methods and molecular docking approach to study anticancer drugs and hemoglobin interaction. For this purpose, we prepared self-assembled monolayers (SAMs) of thiolated hemoglobin on the gold substrate. Electrochemically active chemo drugs, i. e., doxorubicin, withaferin-a, and 5-fluorouracil, are selected and allowed to interact with SAMs of hemoglobin at the physiological condition to study the redox activity and impedimetric behavior. Doxorubicin and withaferin-a show similar behavior in cyclic voltammetry and impedance spectroscopic, i. e., redox process due to hydroquinone/quinone/ketone ring, and faster interfacial electro-transfer kinetics and decreasing in electrontransfer resistance with increasing concentration. In contrast, 5fluorouracil shows only the oxidation reaction. The molecular docking studies were in good agreement with the electrochemical study. All selected anticancer drugs are found to bind hemoglobin, with doxorubicin showing maximum binding efficiency and 5-fluorouracil showing the least. Doxorubicin's highest binding sites contain Tyr 145, which may be involved in the electron transport pathway between doxorubicin and hemoglobin, while Tyr35 in withaferin-a, but absent in case of 5-fluorouracil.

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Probing the biological evaluations of a new designed Pt(II) complex using spectroscopic and theoretical approaches: human hemoglobin as a target

Cited by 39 publications

References 54 publications

The Synergistic Combination of Cisplatin and Piperine Induces Apoptosis in MCF-7 Cell Line

The Synergistic Combination of Cisplatin and Piperine Induces Apoptosis in MCF-7 Cell Line

Alteration of connexins gene expression by silibinin during hepatic warm ischemia-reperfusion injury in the rat model

Study of Anticancer Drugs Interaction with Hemoglobin by Electrochemical Methods and Molecular Docking: Implications towards Anticancer Treatment

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