Journal of King Saud University: Science (Feb 2024)

Pinostrobin attenuated cadmium instigated cardiotoxicity in albino rats: A biochemical, inflammatory, apoptotic and histopathological examination

  • Mehrab Khalil,
  • Muhammad Faisal Hayat,
  • Moazama Batool,
  • Mukhtar Ahmed,
  • Mian Nadeem Riaz

Journal volume & issue
Vol. 36, no. 2
p. 103074

Abstract

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Cadmium (Cd) is a noxious and non-biodegradable heavy metal which instigates various organ toxicities such as cardiac injuries. Pinostrobin (PSB) is a potent dietary bioflavonoid, which shows various pharmacological potentials. The current research was designed to evaluate the ameliorative effects of PSB against Cd elicited cardiac dysfunction in rats. Twenty-four albino rats were apportioned into four equal groups viz. control, Cd (5 mg/kg), Cd (5 mg/kg) + PSB (40 mg/kg) and PSB (40 mg/kg) only treated group. It was observed that Cd intoxication reduced catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), activities and glutathione S-transferase (GST) contents while escalating the levels of reactive oxygen species (ROS), hydrogen peroxide (H2O2) and malondialdehyde (MDA). Furthermore, Cd exposure escalated the levels of cardiac injury markers such as creatine phosphokinase (CPK), creatine kinase-myocardial band (CK-MB), troponin I and lactate dehydrogenase (LDH). Besides, the levels of inflammatory cytokines nuclear factor- κB (NF-κB), interleukin 1beta (IL-1ß), tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activity were upregulated in Cd intoxicated group. Similarly, Caspase-3, Bax and Caspase-9 levels were augmented, and Bcl-2 levels were reduced after Cd administration. In addition, the histopathological examination revealed a notable cardiac tissue impairment in the Cd exposed group. Nonetheless, PSB treatment significantly (p < 0.05) recovered the abovementioned Cd-induced impairments. Therefore, the current study revealed that PSB might be a promising ameliorative agent to ameliorate Cd instigated cardiac damages.

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