Abstract
Background:
The metabolism of toxins after ingestion by animals involves transformation into various metabolites with different levels of toxicity. Aflatoxin B1 undergoes biotransformation into various compounds in the mitochondria that are closely related to its toxic effects. Capsicum annuum L. or chili is a plant that produces a spicy taste and sharp aroma produced by capsaicinoid compounds. Capsaicin in vitro has been shown to have effects on various cell types, including prostate cells, cells that undergo proliferation in the stomach, and hepatocytes, without causing significant side effects on normal cells.

Aim:
This study aimed to determine whether capsaicin inhibits the expression of alpha serine/threonine-protein kinase 1(AKT1) and mitogen-activated protein kinase 1 (MAPK1) target proteins in vivo by scoring using immunohistochemistry (IHC) and histopathological hepatic staining hematoxylin-eosin (HE).

Methods:
IHC was performed by counting the number of transformed cells using monoclonal antibodies and liver pathogenicity was assessed by scoring hepatic lesions (congestion, degeneration, and necrosis) using HE staining preparations.

Results:
Capsaicin treatment significantly reduced liver damage and aflatoxin B1-induced protein expression. Histopathological scores for degeneration, congestion, and necrosis were significantly lower in the aflatoxin B1 (AFB1) + capsaicin group (P3: 15.42 ± 0.65, 15.50 ± 0.50, 15.50 ± 0.58) than in the AFB1-only group (P2: 21.50 ± 0.57 for all variables; p < 0.05). Immunohistochemical analysis showed that capsaicin co-treatment decreased AKT1 (P3: 16.33 ± 0.69 vs. P2: 19.75 ± 0.56) and MAPK1 expression (P3: 13.83 ± 0.61 vs. P2: 20.00 ± 0.34), with a statistically significant reduction in MAPK1 expression (p < 0.05).

Conclusion:
Capsaicin demonstrated a protective effect by reducing liver damage and downregulating AKT1 and MAPK1 expression in mice with aflatoxin B1-induced hepatotoxicity.

Key words: Capsaicin; Aflatoxin B1; AKT1; MAPK1; Good health and well being.