Cadmium-induced hepatorenal toxicity: Protective role of Aframomum melegueta and Rauvolfia vomitoria via NFκB and IL-1β Pathway Modulation

Abstract

Introduction: Cadmium, classified as a Group I human carcinogen by the International Agency for Research on Cancer [IARC], induces toxicity primarily through oxidative stress driven by the excessive reactive oxygen species [ROS] generation, triggering inflammatory responses and causes multi-organ damage, particularly in the liver and kidneys. This study evaluated the histopathological and molecular changes associated with cadmium chloride [CdCl₂]-induced hepatorenal toxicity and the protective effects of methanolic extracts of Aframomum melegueta and Rauvolfia vomitoria in adult male Wistar rats.

Methods: Twenty-five rats weighing 200 g each were randomly assigned to five groups [n = 5]. Group I was administered only distilled water without CdCl2 exposure, while Groups II–V received CdCl₂ [12 mg/kg body weight] by oral gavage once weekly. Group II remained untreated, Groups III and IV received R. vomitoria or A. melegueta, respectively, at a dose of 200 mg/kg body weight, while Group V received a combined treatment of both extracts. After 28 days, liver and kidney tissues were collected for histopathological examination and mRNA expression analysis of nuclear factor kappa B [NFκB] and interleukin-1 beta [IL-1β].

Results: CdCl₂ exposure significantly increased NFκB and IL-1β expression [p < 0.05], indicating enhanced inflammatory signalling response and tissue injury. Treatment with either A. melegueta or R. vomitoria significantly downregulated these pro-inflammatory markers and ameliorated CdCl₂-induced histopathological damage. However, co-administration of both extracts did not produce additional protective effects.

Conclusion: A. melegueta and R. vomitoria individually attenuate CdCl₂-induced hepatorenal toxicity by modulating NFκB and IL-1β pathways, while their combined use offers no added benefit.