The Effect of Cisplatin Toxicity and Capsaicin on Electron Transport Chain in Liver and Kidney of Sprague Dawley Rats

Kursunluoglu, Gizem; Kayalı, Hülya Ayar; Taşkıran, Dilek

doi:10.1007/s12013-014-9857-z

Cited by 24 publications

(9 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The dose of CIS used to induce renal damage in this study (5 mg/kg) was selected based on previous literature (El-Garhy et al, 2014;Kursunluoglu et al, 2014). The doses of UA and EA were selected based on prior studies (Espín et al, 2013;García-Niño and Zazueta, 2015) as well as keeping in mind the translational feasibility of conventional dosage forms for oral administration (50 mg/kg, human equivalent dose:∼520 mg for 65 kg person) (Food and Drug Administration, 2005).…”

Section: Discussionmentioning

confidence: 99%

Urolithin A Mitigates Cisplatin-Induced Nephrotoxicity by Inhibiting Renal Inflammation and Apoptosis in an Experimental Rat Model

Guada

Ganugula

Vadhanam

et al. 2017

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Cumulative kidney toxicity associated with cisplatin is severe and there is no clear consensus on the therapeutic management of the same. The pathogenesis involves activation of inflammatory and apoptotic pathways; therefore, regulating these pathways offers protection. Given the anti-inflammatory and antioxidant effects of urolithin A, a gut microbial metabolite of ellagic acid, our aim was to explore the potential use of urolithin A in the prevention of cisplatin-induced nephrotoxicity in an experimental rat model. For this purpose, animals received a single intraperitoneal dose of cisplatin (5 mg/kg body weight). Six hours prior to cisplatin administration, rats were orally treated with either ellagic acid or urolithin A (50 mg/kg body weight), followed by a daily dose of these compounds during the next 5 days. At the end, plasma and kidneys were collected for analysis. Cisplatin-induced kidney damage was revealed by a significant rise in the plasma creatinine levels accompanied by significant morphologic changes in tubules, T cell Ig and mucin domain-containing protein-1, ionized calcium-binding adapter molecule 1, as well as a marked increase in the number of apoptotic cells localized in tubules. Cisplatin also reduced nitric oxide synthase 3 and nuclear factor kappa-light-chain-enhancer of activated B cells resulting in regulation of various inflammatory cytokines. Urolithin A effectively attenuated cisplatin-induced kidney damage and showed significantly greater effect than its precursor ellagic acid on preserving the normal kidney architecture by downregulating the proinflammatory cytokines. In summary, urolithin A mitigates cisplatin-induced nephrotoxicity in rats by modulation of the inflammatory cascade and inhibition of the proapoptotic pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Urolithin A Mitigates Cisplatin-Induced Nephrotoxicity by Inhibiting Renal Inflammation and Apoptosis in an Experimental Rat Model

Guada

Ganugula

Vadhanam

et al. 2017

J Pharmacol Exp Ther

View full text Add to dashboard Cite

show abstract

“…Cisplatin (DDP) is also a well-known anti-cancer drug commonly used for a variety of cancers, including malignancies of bones, soft tissues, blood vessels, and muscles (Dosoize and Madoulet, 2002). DDP also exhibits many adverse effects like other chemotherapeutic agents, including nephrotoxicity, neurotoxicity, and hepatotoxicity (Kursunluoglu et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Thymoquinone Selectively Induces Hepatocellular Carcinoma Cell Apoptosis in Synergism With Clinical Therapeutics and Dependence of p53 Status

Jehan

Chen

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Thymoquinone (TQ) is a natural compound extracted from the black seeds of Nigella sativa Linn. belonging to the Ranunculaceae family. TQ exhibits anti-inflammatory and antineoplastic activities against various cancers. Many therapeutics in hepatocellular carcinoma (HCC) treatments, such as doxorubicin (DOX) and cisplatin (DDP), exhibit considerable side effects on patients. We investigated cytotoxic effects of TQ, alone or in combination with DDP and DOX to HCC cells. TQ exhibited selective killing to HCC HepG2 and SMMC-7721 cells, but relatively low toxicity to normal liver HL-7702 cells. Importantly, when used with DOX or DDP, TQ showed synergistic inhibition of HCC cells, but not HL-7702 cells. We also discovered that Hep3B cells with a p53 null status were more sensitive to TQ than HepG2 and SMMC-7721 cells harboring wild type p53. Consistently, shRNAmediated p53 silencing in HepG2 cells dramatically enhanced TQ-induced apoptosis, measured by caspase 3 and PARP cleavage. Furthermore, TQ-stimulated increase of reactive oxygen species (ROS) in p53-depleted cells was more pronounced than that in cells with intact p53. In summary, we discovered that TQ synergistically improves the anti-cancer activity of DOX and DDP, and loss of p53 sensitizes HCC cells to TQ-induced apoptosis.

show abstract

“…Unfortunately, chemotherapy treatment strategies give rise to many side effects. DDP, like other therapeutic agents, exhibits several side effects, including hepatotoxicity, nephrotoxicity, neurotoxicity, and ototoxicity [12][13][14]. Hence, new adjuvant agents that potentiate anticancer activities of DDP and counteract its adverse effects are urgently needed.…”

Section: Introductionmentioning

confidence: 99%

Progesterone-Calcitriol Combination Enhanced Cytotoxicity of Cisplatin in Ovarian and Endometrial Cancer Cells In Vitro

et al. 2020

View full text Add to dashboard Cite

Initially, patients that respond to cisplatin (DDP) treatment later relapse and develop chemoresistance. Agents that enhance DDP effectiveness will have a significant impact on cancer treatment. We have shown pronounced inhibitory effects of the progesterone-calcitriol combination on endometrial and ovarian cancer cell growth. Here, we examined whether and how progesterone-calcitriol combination potentiates DDP anti-tumor effects in cancer cells. Ovarian and endometrial cancer cells treated with various concentrations of DDP showed a concentration-dependent decrease in cell proliferation. Concurrent treatment of cells with DDP and progesterone-calcitriol ombination potentiated anticancer effects of DDP compared to DDP-calcitriol, or DDP-progesterone treated groups. The anticancer effects were mediated by increased caspase-3, BAX, and decreased BCL2 and PARP-1 expression in DDP and progesterone-calcitriol combination-treated cells. Stimulation of the PI3K/AKT and MAPK/ERK pathways seen in cancer cells was reduced in DDP-progesterone-calcitriol treated cells. Pretreatment of cells with specific inhibitors further diminished AKT and ERK expression. Furthermore, progesterone-calcitriol potentiated the anti-growth effects of DDP on cancer cells by attenuating the expression of SMAD2/3, multidrug resistance protein- 1 (MDR-1), and ABC transporters (ABCG1, and ABCG2), thereby impeding the efflux of chemo drugs from cancer cells. These results suggest a potential clinical benefit of progesterone-calcitriol combination therapy when used in combination with DDP.

show abstract

The Effect of Cisplatin Toxicity and Capsaicin on Electron Transport Chain in Liver and Kidney of Sprague Dawley Rats

Cited by 24 publications

References 40 publications

Urolithin A Mitigates Cisplatin-Induced Nephrotoxicity by Inhibiting Renal Inflammation and Apoptosis in an Experimental Rat Model

Urolithin A Mitigates Cisplatin-Induced Nephrotoxicity by Inhibiting Renal Inflammation and Apoptosis in an Experimental Rat Model

Thymoquinone Selectively Induces Hepatocellular Carcinoma Cell Apoptosis in Synergism With Clinical Therapeutics and Dependence of p53 Status

Progesterone-Calcitriol Combination Enhanced Cytotoxicity of Cisplatin in Ovarian and Endometrial Cancer Cells In Vitro

Contact Info

Product

Resources

About