Osteoporosis (OP) is characterized by the flaccidity of bones or bone bi-disease caused by kidney deficiency. Lindera aggregate has been used to strengthen kidney function in China for thousands of years. It has been approved by Chinese Pharmacopoeia that the root of Lindera aggregata (RLA) can replenish and tonify the kidney, which is thought to be an effective way to alleviate OP. In this study, a network pharmacology approach was applied to explore the active components and potential mechanisms of RLA in osteoporosis treatment. Then, the ethanolic extract of the root of L. aggregata (EERL) was prepared and these predicted results were validated by prednisone-induced zebrafish embryos model. Moreover, the candidate compounds were identified by UPLC-ESI-MS/MS. The anti-OP results showed that EERL could significantly reverse the bone loss of zebrafish induced by prednisone. The mRNA expressions results showed that EERL decreased osteoclast bone resorption by regulating the RANK/RANKL/OPG system. Also, it increased bone formation by regulating the gene expressions of spp1, mmp2, mmp9, runx2b, alp, and entpd5a. Our results demonstrated the reliability of the network pharmacology method, and also revealed the anti-OP effect and potential mechanism of RLA.
Depression is a common mental illness, which is highly related to intestinal motor dysfunction and causes a global burden of disease. Lindera aggregata (LA), a traditional medicinal herb, has been used to treat gastrointestinal disorders; however, the effect of LA on depression remains unclear. Here, we assessed the impact of LA on chronic unpredictable mild stress (CUMS)-induced depression in mice and explored the related mechanisms. The results showed that LA ameliorated depressive behaviors in mice exposed to CUMS, as evidenced by improved performance in the sucrose preference test, force swimming test, and open field test, as well as increased serum levels of adrenocorticotropic hormone and 5-hydroxytryptamine. In addition, LA increased the serum levels of D-xylose and ghrelin, indicating that LA can promote gastrointestinal motility. Additional studies revealed that LA relieved CUMS-induced hippocampal tissue damage, as shown by hematoxylin and eosin and Nissl staining. LA increased the expression levels of brain-derived neurotrophic factor (BDNF) and promoted the activation of tropomyosin receptor kinase B (TrkB) and cAMP response element-binding (CREB) in the hippocampus of CUMS-exposed mice or in corticosterone-injured HT22 cells. In conclusion, LA can improve CUMS-induced depressive behavior in mice, potentially through hippocampal neuroprotection mediated by the BDNF/TrkB/CREB signaling pathway, which also contributes to improved intestinal function.
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