Prevention and treatment of amygdalin on bone injury in cadmium-exposed rats and its effect on miR-302b-NF-κB-mTOR signaling pathway

Abstract

Abstract: Objective To investigate the preventive effect of amygdalin on bone damage in cadmium poisoning rats and its effect on microRNA-302b（miR-302b）-nuclear factor kappa-B（NF-κB）-rapamycin target protein（mTOR） signaling pathway. Methods Totally 100 clean-grade SD rats were divided into the control group,the cadmium exposure model group（30 mg/kg cadmium dichloride）,amygdalin low,medium and high dose groups（50.0,100.0,200.0 mg/kg）. The rats in the cadmium exposure model group,and the low-,middle- and high-dose amygdalin groups were given daily intraperitoneal injection of cadmium dichloride solution for 12 weeks. During this period,the rats in the low-,medium- and high-dose amygdalin groups were given the corresponding doses of amygdalin by gavage every day. The bilateral femoral tissues were obtained after the experiment,to measure the bone density（BMD）,trabecular number,trabecular thickness,trabecular dispersion,and femoral osteocalcin（OC） of the distal femur,as well as the levels of osteopontin（OPN）,osteoprotegerin（OPG）,femoral miR-302b,NF-κB,mTOR. Results Compared with the control group,the femoral BMD,trabecular number,trabecular thickness,femoral OC,OPN,OPG,and miR-302b levels in the cadmium exposure model group were significantly decreased（all P<0.05）,and the trabecular bone dispersion,femoral NF-κB,mTOR mRNA protein levels were significantly increased（all P<0.05）. Compared with the cadmium exposure model group,the femoral BMD[（1.21±0.19） vs （1.38±0.23）（1.55±0.26）（1.61±0.27）g/cm³],trabecular number[（2.36±0.39） vs （3.98±0.67）（4.69±0.78）（5.87±0.94）/mm²],trabecular thickness[（0.04±0.01） vs（0.07±0.01）（0.09±0.02）（0.12±0.02）mm],femoral OC[（328.91±105.85） vs （585.25±184.20）（895.25±298.52）（1 250.21±358.52）moL/mg）],OPN[（589.52±185.54） vs （854.29±258.22）（1 358.96±420.59）（1 852.20±595.20）moL/mg],OPG[（485.63±121.65） vs （741.25±222.69）（1 259.95±489.52）（1 752.63±652.85）moL/mg],miR-302b（0.69±0.11 vs 0.95±0.16,1.29±0.21,1.65±0.26） were significantly increased（all P<0.05）. And the trabecular bone dispersion[（0.68±0.14） vs （0.52±0.11）（0.48±0.09）（0.31±0.07）mm],femoral NF-κB（3.56±0.73 vs 1.37±0.21,2.90±0.41,2.02±0.23,0.95±0.48 vs 0.87±0.14,0.72±0.25,0.43±0.12）,mTOR mRNA protein levels（4.37±0.76 vs 3.52±0.25,2.57±0.65,1.55±0.21,1.02±0.36 vs 0.82±0.47,0.68±0.54,0.38±0.35） were significantly decreased（all P<0.05）. With an increase in the dosage of amygdalin administration,the BMD,trabecular number,trabecular thickness,femoral OC,OPN,OPG,and miR-302b levels in the amygdalin groups gradually increased,while the trabecular bone dispersion,femoral NF-κB,and mTOR mRNA protein levels gradually decreased,with a significant dose response relationship（all P<0.05）. Conclusion The amygdalin can significantly improve the number of trabecular bone structures,increase bone mineral density,and have a significant therapeutic effect on cadmium-exposed bone injury,its mechanism is related to the activation of miR-302b by amygdalin and the inhibition of NF-κB and mTOR expression.

Key words: Amygdalin, Cadmium, Bone, MicroRNA-302b, Nuclear factor kappa-B, Rapamycin target protein

CLC Number:

R-332

BAI Yang, ZHANG Debing, WANG Shanan, QI Shipeng. Prevention and treatment of amygdalin on bone injury in cadmium-exposed rats and its effect on miR-302b-NF-κB-mTOR signaling pathway. [J]OCCUPATION AND HEALTH, 2023, 39(13): 1733-1739.

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