Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2026
Investigation of molecular effects of beta caryophyllene in cadmium-induced nephrotoxicity model in rats: in silico and in vivo studies.
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Sağlam Yavuz Selim, Orhan Betül, Çinar Burak, Gözegi̇r Berrah, Çomakli Selim, Teki̇n Samet, Bolat Merve, Bolat İsmail
Аннотация
BACKGROUND: Cadmium is one of the toxic heavy metals that accumulate in the kidneys, and it can cause kidney damage by triggering oxidative stress, ER stress, inflammation, and apoptosis. β-caryophyllene (BCP) is a volatile ingredient found in various spice essential oils, known for its anti-inflammatory and strong oxygen-free radical scavenging properties. In this study, we aimed to test the effects of BCP on kidney damage caused by Cd administration.
METHODS: Adult male Sprague Dawley (n = 35) were divided to the five following groups (n = 7/group): control group, BCP group that received BCP intragastric for 7 days (400 mg/kg/day), Cd group that received CdCl2 intraperitoneal injections for 7 days (6.5 mg/kg/day), and rats that received Cd simultaneously with small (200 mg/kg/day) and high doses (400 mg/kg/day) of BCP.
RESULTS: BCP significantly reduced lipid peroxidation, restored reduced glutathione (GSH), superoxide dismutase (SOD) levels and catalase activity, decreased the elevations of Toll-like receptor 4 (TLR-4), nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), IL-1β in cadmium-induced kidney injury. Histopathological examination showed that cadmium-induced kidney injury was attenuated by BCP treatment. Immunohistochemical and immunofluorecence analysis showed that BCP significantly decreased the cadmium-induced overexpression of Keap-1, Bax, and caspase-3, increased the cadmium-induced downexpression of Bcl-2, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in kidney tissues. BCP also markedly mitigated ER stress (GRP78, ATF4, ATF6, and CHOP expressions).
CONCLUSION: Thus, BCP may protect kidney tissues from Cd-induced nephrotoxicity by regulating oxidant/antioxidant status, reducing inflammation, ER stress, cell death, and activating the Nrf2/HO-1 signaling pathway.
METHODS: Adult male Sprague Dawley (n = 35) were divided to the five following groups (n = 7/group): control group, BCP group that received BCP intragastric for 7 days (400 mg/kg/day), Cd group that received CdCl2 intraperitoneal injections for 7 days (6.5 mg/kg/day), and rats that received Cd simultaneously with small (200 mg/kg/day) and high doses (400 mg/kg/day) of BCP.
RESULTS: BCP significantly reduced lipid peroxidation, restored reduced glutathione (GSH), superoxide dismutase (SOD) levels and catalase activity, decreased the elevations of Toll-like receptor 4 (TLR-4), nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), IL-1β in cadmium-induced kidney injury. Histopathological examination showed that cadmium-induced kidney injury was attenuated by BCP treatment. Immunohistochemical and immunofluorecence analysis showed that BCP significantly decreased the cadmium-induced overexpression of Keap-1, Bax, and caspase-3, increased the cadmium-induced downexpression of Bcl-2, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in kidney tissues. BCP also markedly mitigated ER stress (GRP78, ATF4, ATF6, and CHOP expressions).
CONCLUSION: Thus, BCP may protect kidney tissues from Cd-induced nephrotoxicity by regulating oxidant/antioxidant status, reducing inflammation, ER stress, cell death, and activating the Nrf2/HO-1 signaling pathway.