Cuscuta chinensis Ameliorates Immunosuppression and Urotoxic Effect of Cyclophosphamide by Regulating Cytokines - GM-CSF and TNF-Alpha

Abstract

Cancer is the leading cause of death worldwide. Cyclophosphamide (CTX) is commonly used as anticancer drug which causes toxicity by its reactive metabolites such as acroline and phosphoramide mustard. In this study, Cuscuta chinensis (C. chinensis) (family: Convolvulaceae) was assessed for ability to restore mice against CTX-induced toxicity. Coadministration of C. chinensis extract (10 mg/kg BW, IP, daily) for ten consecutive days reduced CTX-induced (25 mg/kg BW, IP, daily) toxicity. Treatment with C. chinensis extract significantly (p < 0.01) increased the relative organ weight and body weight. Moreover, administration of C. chinensis extract significantly increased bone marrow cellulatity and α-esterase activity in CTX-treated mice which suggested its protective role on the hematopoietic system. The GSH content was drastically reduced by CTX administration in urinary bladder which was enhanced by treatment with C. chinensis extract, indicating that preventing acroline-mediated tissue damage or cell toxicity and also the extract decreased the urinary bladder nitric oxide (NO) level which proves recovery over urinary tract injury associated with CTX treatment. The administration of C. chinensis extract decreased serum urea, creatinine, and bilirubin levels when compared to CTX-alone-treated group. Histopathological analysis of the urinary bladder of CTX-alone-treated group showed necrotic damage whereas the C. chinensis-treated group showed normal bladder architecture. The above data clearly demonstrates chemoprotective role of C. chinensis against CTX-induced toxicities by regulating antioxidant and inflammatory mediators.

Kunxian Capsule for Rheumatoid Arthritis: Inhibition of Inflammatory Network and Reducing Adverse Reactions Through Drug Matching

“…Total flavonoids of Epimedium protect the reproductive system against cyclophosphamide-induced toxicity by inhibiting oxidative stress (Yuan et al, 2014). By contrast, Cuscuta chinensis Lam detoxicates cyclophosphamide-induced toxicity through regulating cytokines GM-CSF and TNF-a (Raju et al, 2015). Herein, for endeavoring to illustrate the coexisting mechanism of causing and alleviating side effects, we supposed amino acid and nucleotide metabolism approach.…”

All-trans retinoic acid has renoprotective effects on Cisplatin-induced acute kidney injury in rats.

“…Cisplatin injection is also associated with renal inflammation and fibrogenesis as mentioned above, NF-kB has an expressing role for pro-inflammatory genes such as cytokines, chemokines, and adhesion molecules, so it can be expressed as a potential target for testing any anti-inflammatory agent [36], the elevated level of NF kB after cisplatin injection can be explained by the fact that, cisplatin induce the phosphorylation of NF kB and degrading the inhibitory protein IkB α and subsequently, it facilitates the translocation of NF kB to the nucleus, and hence increasing its gene expression level [37], in the present study, injection of cisplatin increased NF kB mRNA gene expression in cisplatin group compared with control group, which was in agreement with previous study performed by Bayomi, et al, (2013) [38]. By contrast, in ATRA treated group, the present results revealed that, ATRA markedly reduced NF kB mRNA gene expression compared with cisplatin group, Consistent with these findings, Rao et al, 2013, documented that ATRA was able to ameliorate liver injury in a liver I/R model by inhibiting NF-kB activation by suppressing the phosphorylation of NF kB , suppressing the degradation of IkBa protein, decreasing neutrophil recruitment and activity and decreasing inflammatory cytokine levels [39].…”

Administration of Adipose derived mesenchymal stem cells promotes amelioration of renal function in cisplatin-induced acute kidney injury in rats.

“…Signaling pathway of NF kB as well as its expression role for pro-inflammatory genes such as cytokines and chemokines can explain the renal inflammatory mechanism [26], also the above reasons made it a potential target to test any anti-inflammatory agent [27]. Cisplatin can degrade the inhibitory protein IkB α , which facilitates the phosphorylation process of NF kB and hence its translocation to the nucleus [28].…”