Tissue & cell · 2026
Lepidium meyenii (maca) attenuates titanium dioxide nanoparticle-induced hepatotoxicity in rats.
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ElSawy Naser A, Soliman Nada Mohamed Mohamed, Ali Sahar K, Algazeery Ahmed, Dahran Naief A, Filfilan Reham M, AlGifry Hawazen A, Saleh Alaa M, Mohamed Noura Mostafa, Elkattawy Hany A
Аннотация
BACKGROUND AND OBJECTIVE: Titanium dioxide nanoparticles (TiO₂-NPs) have been implicated in liver injury through oxidative stress and inflammatory mechanisms. This study aimed to investigate whether Lepidium meyenii (maca) can attenuate TiO₂-NPs-induced hepatotoxicity in rats.
METHODS: Thirty-two adult male rats were randomly assigned to four groups: control, Lepidium meyenii, TiO₂-NPs, and TiO₂-NPs plus Lepidium meyenii. Animals were randomly assigned to experimental groups, and the outcome assessment was performed in a blinded manner. Hepatic toxicity was evaluated using serum liver function tests (alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), total protein, albumin, and globulin); lipid peroxidation marker (malondialdehyde (MDA); antioxidant enzyme activities (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT)); inflammatory and anti-inflammatory mediators (interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and nitric oxide synthase (iNOS) expression); and apoptotic markers (B-cell lymphoma 2 (BCL-2), BCL-2-associated X protein (BAX), p53, and caspase-3 expression). Histopathological examination was performed.
RESULTS: TiO₂-NPs (150 mg/kg, intraperitoneally for 14 days) significantly increased ALT, AST, and ALP levels and reduced total protein, albumin, and globulin levels (p < 0.05 vs. control). TiO₂-NPs also increased MDA and decreased SOD, GSH-Px, and CAT activities (p < 0.05 vs. control). Inflammatory responses were enhanced, as shown by elevated IL-6 and TNF-α, reduced IL-10, and increased iNOS expression. In addition, TiO₂-NPs upregulated BAX, p53, and caspase-3 and downregulated BCL-2, accompanied by marked histopathological liver damage (p < 0.001 vs. control). In contrast, Lepidium meyenii (500 mg/kg, orally for 35 days) significantly ameliorated these changes, improving liver function, suppressing oxidative stress, apoptosis, and inflammation, and preserving hepatic architecture.
CONCLUSION: Lepidium meyenii mitigated TiO₂-NPs-induced hepatic damage in rats, suggesting a potential protective role that warrants further investigation in additional preclinical and translational studies.
METHODS: Thirty-two adult male rats were randomly assigned to four groups: control, Lepidium meyenii, TiO₂-NPs, and TiO₂-NPs plus Lepidium meyenii. Animals were randomly assigned to experimental groups, and the outcome assessment was performed in a blinded manner. Hepatic toxicity was evaluated using serum liver function tests (alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), total protein, albumin, and globulin); lipid peroxidation marker (malondialdehyde (MDA); antioxidant enzyme activities (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT)); inflammatory and anti-inflammatory mediators (interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and nitric oxide synthase (iNOS) expression); and apoptotic markers (B-cell lymphoma 2 (BCL-2), BCL-2-associated X protein (BAX), p53, and caspase-3 expression). Histopathological examination was performed.
RESULTS: TiO₂-NPs (150 mg/kg, intraperitoneally for 14 days) significantly increased ALT, AST, and ALP levels and reduced total protein, albumin, and globulin levels (p < 0.05 vs. control). TiO₂-NPs also increased MDA and decreased SOD, GSH-Px, and CAT activities (p < 0.05 vs. control). Inflammatory responses were enhanced, as shown by elevated IL-6 and TNF-α, reduced IL-10, and increased iNOS expression. In addition, TiO₂-NPs upregulated BAX, p53, and caspase-3 and downregulated BCL-2, accompanied by marked histopathological liver damage (p < 0.001 vs. control). In contrast, Lepidium meyenii (500 mg/kg, orally for 35 days) significantly ameliorated these changes, improving liver function, suppressing oxidative stress, apoptosis, and inflammation, and preserving hepatic architecture.
CONCLUSION: Lepidium meyenii mitigated TiO₂-NPs-induced hepatic damage in rats, suggesting a potential protective role that warrants further investigation in additional preclinical and translational studies.