Silymarin alleviates docetaxel-induced central and peripheral neurotoxicity by reducing oxidative stress, inflammation and apoptosis in rats

Yardım, Ahmet; Küçükler, Sefa; Özdemir, Selçuk; Çomaklı, Selim; Çağlayan, Cüneyt; Kandemir, Fatih Mehmet; Çelik, Hamit

doi:10.1016/j.gene.2020.145239

Cited by 62 publications

(33 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In MWM, DTX-treated rats reported a reduction in the time spent in the target quadrant but not significantly compared with the control group (Fardell et al 2013a). A single dose of DTX (30 mg/kg, i.p) in male Sprague-Dawley rats increased the levels of MDA, p38α, MAPK, TNF-α, GFAP, and NF-κB and decreased the levels of glutathione, SOD, catalase, Nrf-2, NCAM (neural cell adhesion molecule), and HO1 (Yardım et al 2020).…”

Section: Docetaxelmentioning

confidence: 86%

Animal models of chemotherapy-induced cognitive decline in preclinical drug development

et al. 2021

View full text Add to dashboard Cite

Rationale Chemotherapy-induced cognitive impairment (CICI), chemobrain, and chemofog are the common terms for mental dysfunction in a cancer patient/survivor under the influence of chemotherapeutics. CICI is manifested as short/long term memory problems and delayed mental processing, which interferes with a person’s day-to-day activities. Understanding CICI mechanisms help in developing therapeutic interventions that may alleviate the disease condition. Animal models facilitate critical evaluation to elucidate the underlying mechanisms and form an integral part of verifying different treatment hypotheses and strategies. Objectives A methodical evaluation of scientific literature is required to understand cognitive changes associated with the use of chemotherapeutic agents in different preclinical studies. This review mainly emphasizes animal models developed with various chemotherapeutic agents individually and in combination, with their proposed mechanisms contributing to the cognitive dysfunction. This review also points toward the analysis of chemobrain in healthy animals to understand the mechanism of interventions in absence of tumor and in tumor-bearing animals to mimic human cancer conditions to screen potential drug candidates against chemobrain. Results Substantial memory deficit as a result of commonly used chemotherapeutic agents was evidenced in healthy and tumor-bearing animals. Spatial and episodic cognitive impairments, alterations in neurotrophins, oxidative and inflammatory markers, and changes in long-term potentiation were commonly observed changes in different animal models irrespective of the chemotherapeutic agent. Conclusion Dyscognition exists as one of the serious side effects of cancer chemotherapy. Due to differing mechanisms of chemotherapeutic agents with differing tendencies to alter behavioral and biochemical parameters, chemotherapy may present a significant risk in resulting memory impairments in healthy as well as tumor-bearing animals.

show abstract

Section: Docetaxelmentioning

confidence: 86%

Animal models of chemotherapy-induced cognitive decline in preclinical drug development

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Besides, inflammation is a major cause of impaired functions in the nervous system (Wang et al., 2018). A recent study reported that silymarin therapy relieves docetaxel‐induced injury of central nervous system by suppressing inflammation (Yardım et al., 2021). Moreover, the application of curcumin was also found to alleviate damage in neuronal cells by inhibiting inflammation and modulating the Wnt/β‐catenin pathway (Zhou et al., 2020).…”

Section: Discussionmentioning

confidence: 99%

Atractylenolide III alleviates isoflurane‐induced injury in rat hippocampal neurons by activating the PI3K/Akt/mTOR pathway

Zhu

Wang

et al. 2021

J Food Biochem

View full text Add to dashboard Cite

The use of anesthetics relieves discomfort in patients during operation, but extensive application of anesthetics can cause damage to the nervous system. Atractylenolide III (ATL‐III) is an active ingredient derived from Baizhu, which is a kind of traditional Chinese medicines. Recent studies have shown that ATL‐III alleviates inflammation and oxidative stress in various tissues by regulating the PI3K/Akt/mTOR signaling pathway. However, whether or not the application of ATL‐III could relieve isoflurane‐induced damage in rat hippocampal neurons remains unclear. In this study, rats were stimulated with isoflurane and treated with ATL‐III (intragastric administration) simultaneously. After rats were sacrificed, apoptosis and autophagy in the hippocampal neurons were assessed using TUNEL assays and western blotting, respectively. Then, the expression of inflammatory factors was determined by q‐PCR and ELISA. The levels of p‐PI3K, p‐Akt, and p‐mTOR were quantified by western blotting. We found that ATL‐III relieved isoflurane‐induced apoptosis, autophagy and inflammation in hippocampal neurons in rats. ATL‐III treatment also inhibited the expression of TNF‐α, IL‐1β, and IL‐6 in these cells. Furthermore, ATL‐III promoted the expression of p‐PI3K, p‐Akt, and p‐mTOR in the hippocampal neurons. All these results indicated that ATL‐III alleviated isoflurane‐induced injury in rat hippocampal neurons by activating the PI3K/Akt/mTOR signaling pathway. Practical applications Whether or not Atractylenolide III (ATL‐III) could alleviate neurotoxicity induced by anesthetics is unclear. In this study, we investigated the effect of ATL‐III on anesthetic‐induced nervous system damage. The findings from this study could also provide a novel therapy for the treatment of patients with anesthetic‐induced nerve injury.

show abstract

“…However, the excessive occurrence of apoptosis in testicular tissues can lead to infertility in men due to some factors (Richburg, 2000). Caspase‐3, one of the cysteine aspartic acid protease family members, has an important role in the apoptosis pathway (Metwally et al., 2020; Yardim et al., 2020; Yardım et al., 2020), and heavy metals are known to cause apoptosis by initiating caspase‐3 activation. (Wang et al., 2017).…”

Section: Discussionmentioning

confidence: 99%

Chrysin protects against testicular toxicity caused by lead acetate in rats with its antioxidant, anti‐inflammatory, and antiapoptotic properties

et al. 2020

Self Cite

View full text Add to dashboard Cite

In the present study, the protective effects of chrysin (CHR) against testicular damage caused by lead acetate (PbAc) were examined. In this way, 30 min after rats were given 25 and 50 mg/kg/b.w CHR orally for seven consecutive days, 30 mg/kg/b.w PbAc was administered orally. In biochemical analysis of testicular tissue, it was found that PbAc-reduced antioxidant parameters [glutathione peroxidase (GPx), glu

show abstract

Silymarin alleviates docetaxel-induced central and peripheral neurotoxicity by reducing oxidative stress, inflammation and apoptosis in rats

Cited by 62 publications

References 59 publications

Animal models of chemotherapy-induced cognitive decline in preclinical drug development

Animal models of chemotherapy-induced cognitive decline in preclinical drug development

Atractylenolide III alleviates isoflurane‐induced injury in rat hippocampal neurons by activating the PI3K/Akt/mTOR pathway

Chrysin protects against testicular toxicity caused by lead acetate in rats with its antioxidant, anti‐inflammatory, and antiapoptotic properties

Contact Info

Product

Resources

About