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| Effects of atmospheric particulate matter PM2.5 on bone metabolism in aged male rats |
| ZHANG Baoyu* YIN Ruili* MO Caiyan ZHAO Dong MA Yan KE Jing |
| Center for Endocrine Metabolism and Immune Diseases, Beijing Luhe Hospital, Capital Medical University, Beijing 100149, China |
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Abstract Objective To observe the effect of atmospheric fine particulate matter PM2.5 on bone mineral density and trabecular structure of aged male rats, and the effect of receptor activator of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin (OPG) expression of function, and to explore PM2.5 effect on bone metabolism of aged rats. Methods A total of 20 male SD rats aged 19 months were divided into the cleaning group and the PM2.5 group according to the random number table method using a haze warehouse exposure system, with 10 rats in each group. They were kept in a clean warehouse and a haze warehouse respectively, and their weight was monitored weekly. After 12 weeks, femoral tissue was collected and bone mineral density of rats was detected. Bone morphology was observed by hematoxylin-eosin (HE) staining. The mRNA in bone marrow was extracted and the expression of RANKL/OPG was detected by Real-time PCR. Results The body weight of the two groups increased steadily with the extension of time, but there was no signifant difference in body weight between the two groups (P ＞ 0.05). HE results showed that compared with the cleaning group, the bone trabeculae in the cancellous bone of the PM2.5 group were reduced, arranged sparsely and partially fractured. Compared with the clean group, bone mineral density, trabecular number, trabecular area and percentage of trabecular area in the PM2.5 group all decreased significantly, with statistically significant differences (P ＜ 0.05 or P ＜ 0.01). Real-time PCR results showed that compared with the clean group, OPG mRNA content in the PM2.5 group was decreased, while RANKL mRNA content was increased, with statistically significant differences (all P ＜ 0.05). Conclusion Long-term exposure to PM2.5 may increase osteoclast activity by increasing the expression of osteoblasts RANKL and decreasing the expression of OPG, thereby reducing bone mineral density and bone trabeculae and aggravating osteoporosis in aged rats.
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