Ferula assa-foetida Ameliorates Lead Acetate-induced Splenotoxicity and Hematological Disturbances in Rats via Enhancement of Antioxidant Defense and Suppression of Inflammatory Cytokines
Athare Dehghan, Seyyed Majid Bagheri, Mansour Esmailidehaj, Maryam Yadegari, Seyed Mahdi Mohamadi-ZarchIntroduction:
Lead poisoning poses a significant global health challenge, impairing immune function and inducing oxidative stress and inflammation, particularly in the spleen. Ferula assa-foetida, a traditional medicinal plant, exhibits antioxidant and anti-inflammatory properties, but its protective effects against lead-induced splenic toxicity remain underexplored. This study evaluates the protective effects of asafoetida on lead-induced splenic toxicity in male Wistar rats, focusing on hematological, biochemical, molecular, and histological outcomes.
Methods:
Forty male Wistar rats were divided into five groups (n=8): control, lead (10 mg/kg/day), and lead + asafoetida (25, 50, 100 mg/kg/day) for 28 days. Hematological parameters, antioxidant enzyme activities (CAT, GSH, SOD), inflammatory gene expression (IL-6, TNF-α, TGF-β), and splenic histopathology were assessed. Data were analyzed using ANOVA and Tukey’s post-hoc test (p <0.05).
Results:
Lead exposure reduced RBC, hemoglobin, hematocrit, and antioxidant enzyme activities while increasing inflammatory gene expression and histopathological damage. Asafoetida treatment, particularly at 100 mg/kg, significantly restored hematological parameters (e.g., RBC: 8.3 ± 0.2 ×106/μL, p < 0.01), enhanced CAT, GSH, and SOD activities (p <0.01), and reduced IL-6, TNF-α, and TGF-β expression (p <0.01). Histologically, asafoetida mitigated white pulp degeneration, vascular congestion, and inflammatory infiltration, with the 100 mg/kg dose showing the most significant improvements.
Discussion:
The results confirm that lead-induced splenic toxicity occurs via oxidative stress and inflammation, consistent with prior studies. Asafoetida, especially at 100 mg/kg, exerted dose-dependent protection by restoring antioxidant defenses, suppressing pro-inflammatory cytokines, and improving splenic histology. These effects likely stem from its bioactive compounds (e.g., polyphenols and sulfur derivatives). Similar protective roles of asafoetida have been reported against other heavy metals. Further research is warranted to clarify mechanisms and optimal dosing.
Conclusion:
Asafoetida effectively ameliorates lead-induced splenic toxicity through its antioxidant and anti-inflammatory properties, supporting its potential as a complementary therapy for heavy metal toxicity. Further studies are needed to optimize dosing and elucidate mechanisms.