Apigeninidin-enriched Sorghum bicolor (L. Moench) extracts alleviate Aflatoxin B₁-induced dysregulation of male rat hypothalamic-reproductive axis

Abstract

We examined the protective effect of the apigeninidin (API)-enriched fraction from Sorghum bicolor sheaths extracts (SBE-05, SBE-06, and SBE-07) against aflatoxin B1 (AFB1)-induced dysregulation of male rat’s reproductive system that may trigger infertility. Male rats (160 ± 12 g) were treated with AFB1 (50 µg/kg) along with 5 or 10 mg/kg of SBE-05, SBE-06, and SBE-07 for 28 days. Subsequently, we assessed the reproductive hormone—prolactin, FSH, LH, testosterone levels, and testicular function enzymes. Moreover, we examined rats’ testes, epididymis, and hypothalamus for oxidative and inflammatory stress biomarkers, caspase-9 activity and tissues pathology. We observed that comparative to AFB1 alone treated rats, API co-treatment significantly ( p < 0.05) abated the AFB1-mediated decrease in prolactin and antioxidant defenses and lessened lipid peroxidation (LPO) and reactive oxygen and nitrogen species levels in the examined organs—testes, epididymis, and hypothalamus. API abated AFB1-induced hormone decreases—testosterone, FSH, and LH; and caused improvement in sperm quantity and quality. API lessened AFB1-mediated increase in pro-inflammatory cytokine, increased interleukin-10 level, an anti-inflammatory cytokine and reduced caspase-9 activities. In addition, API reduced alterations in the examined tissue histology. Our findings suggest that S. bicolor API-enrich extracts have active antioxidative, antiapoptotic, and anti-inflammatory activities, which can protect against AFB1-induced dysfunction of the hypothalamic–pituitary–gonadal axis.

The Hydrophobic Extract of Sorghum bicolor (L. Moench) Enriched in Apigenin-Protected Rats against Aflatoxin B1-Associated Hepatorenal Derangement

“…The concomitant effects of AFB 1 -induced toxicities include growth retardation, malnutrition, and immune suppression [ 15 , 16 ]. Efforts to reduce AFB 1 contamination in food products have continually waned due to the recalcitrant nature of the fungal species that mediate the biosynthesis of mycotoxins [ 38 , 39 ] and the induction of metabolic pathways for the breakdown of AFB 1 [ 30 , 33 , 40 ]. Bioactive compounds in plants can remediate AFB 1 -mediated toxicities by inhibiting ROS production, resolution of inflammation, and preventing programmed cell death [ 41 , 42 ].…”

“…Compounds extracted from Sorghum have been shown in in vivo and in vitro studies to have therapeutic effects against non-infectious disorders such as obesity, diabetes, dyslipidemia, cardiovascular disease, cancer, and hypertension [ 30 , 32 ]. Extracts from Sorghum enriched in certain phytochemicals such as apigenin (API), luteolin, luteolinidin, and apigeninidin in S. bicolor extracts have been shown to reduce oxidative stress by upregulating antioxidant enzymes while reducing the generation of reactive oxygen species (ROS) [ 30 , 33 , 34 , 35 ]. Based on the structural–activity relationship (SAR), the abilities of these compounds to stall oxidative stress may be attributed to their possession of several aromatic rings and phenolic groups [ 36 ].…”

Accidental lead in contaminated pipe-borne water and dietary furan intake perturbs rats’ hepatorenal function altering oxidative, inflammatory, and apoptotic balance

“…Significant alterations in hepatic and renal levels of these molecules may trigger the onset of inflammation, as observed in cohorts of rats treated with PbAc and Furan. MPO is a member of haem peroxidase expressed on neutrophils and monocytes [ 62 ] and is known to catalyse the conjugation of H 2 O 2 and chloride, to yield hypochlorous acid (HOCl) [ 63 ]. On decomposition, HOCl evolves harmful free radicals such as singlet oxygen ( 1 O 2 ) and .…”

“…Another clinically accepted protocol for ascertaining xenobiotics' toxicities is evaluating a target organ's histoarchitectural features. In this study, treatments with PbAc and Furan abrogated the normal histology of the liver and kidney, and this may be attributed to the increase in the generation of ROS, proinflammatory cytokines, DNA adducts, and a host of other danger-associated molecular patterns (DAMPs) [ 46 , 63 , 73 ]. These molecules are known to trigger the activation and differentiation of pro-inflammatory cells in the hepatic and renal tissues, leading to the activation of inflammasomes [ 79 , 80 ] and the formation of lesions capable of deranging the liver and kidney of rats.…”