Mitigation of cisplatin induced nephrotoxicity by casticin in male albino rats

Abstract

Cisplatin (CP) is a commonly used, powerful antineoplastic drug, having numerous side effects. Casticin (CAS) is considered as a free radical scavenger and a potent antioxidant. The present research was planned to assess the curative potential of CAS on CP persuaded renal injury in male albino rats. Twenty four male albino rats were distributed into four equal groups. Group-1 was considered as a control group. Animals of Group-2 were injected with 5mg/kg of CP intraperitoneally. Group-3 was co-treated with CAS (50mg/kg) orally and injection of CP (5mg/kg). Group-4 was treated with CAS (50mg/kg) orally throughout the experiment. CP administration substantially reduced the activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione S-transferase (GST), glutathione reductase (GSR), glutathione (GSH) content while increased thiobarbituric acid reactive substances (TBARS), and hydrogen peroxide (H2O2) levels. Urea, urinary creatinine, urobilinogen, urinary proteins, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels were substantially increased. In contrast, albumin and creatinine clearance was significantly reduced in CP treated group. The results demonstrated that CP significantly increased the inflammation indicators including nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activity and histopathological damages. However, the administration of CAS displayed a palliative effect against CP-generated renal toxicity and recovered all parameters by bringing them to a normal level. These results revealed that the CAS is an effective compound having the curative potential to counter the CP-induced renal damage.

Casticin promotes osteogenic differentiation of bone marrow stromal cells and improves osteoporosis in rats by regulating nuclear factor‐κB/mitogen‐activated protein kinase

“…26 Shu-Di-Huang and Gan-Cao inhibits the NF-κB signaling pathway to mediate mesenchymal stem progenitors differentiation. 27 Although CAS was identified to play a part in bladder cancer, 16 skin wound healing 17 and nephrotoxicity, 18 its role and function in osteoporosis maintains to be elucidated. In the current study, we established a rat model of osteoporosis through DEX treatment.…”

“…CAS exerts a protective role on skin wound healing in a rat model 17 . CAS suppresses nephrotoxicity in male albino rats 18 . Although the diverse roles of CAS on different diseases have been identified, whether it is implicated with osteoporosis is unknown.…”

Flavonoids against non-physiologic inflammation attributed to cancer initiation, development, and progression—3PM pathways

“…Data from another preclinical study point out to protective role of quercetin coadministered with vitamin E in the prevention of doxorubicin-induced toxicity in uterine and ovarian tissues in rats [ 209 ]. The administration of casticin in male rats demonstrated a palliative effects against cisplatin-induced renal damage and recovered all renal parameters to normal levels [ 210 ]. Besides cancer, there are also other life-threatening disease/condition in which flavonoids show positive palliative effects.…”