<i>Background</i>. This study used a combination of network pharmacology and experimental confirmation to clarify the mechanism of the compound kidney-invigorating granule (CKG) in treating osteoporosis (OP). <i>Methods</i>. The main bioactive compounds and corresponding targets of CKG were collected and screened via the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), Yet another Traditional Chinese Medicine (YaTCM), and UniProt databases. Disease targets of OP were summarized in GeneCards and the Comparative Toxicogenomics Database (CTD). Targets of CKG for OP were obtained by Venn diagram. The protein-protein interaction (PPI) network was constructed by the STRING database and then screened for hub genes through Cytoscape 3.7.2 software. The Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were analyzed and visualized by R software. Then, CB-Dock was used for molecular docking verification. Finally, we confirmed the antiosteoporosis effect of CKG through animal and cell experiments. <i>Results</i>. A total of 250 putative targets were obtained from 65 bioactive compounds in CKG. Among them, 140 targets were related to OP. Topological analysis of the PPI network yielded 23 hub genes. Enrichment analysis showed the targets of CKG in treating OP might concentrate on the MAPK signaling pathway, the TNF signaling pathway, the PI3K-Akt signaling pathway, etc. The results of molecular docking showed the bioactive components in CKG had good binding ability with the key targets. The experimental results showed that CKG-medicated serum had a promoting effect on proliferating hBMSCs, increasing the expression of AKT, PI3K, ERK1, and IkB in cells and decreasing the expression of IKK in cells. <i>Conclusion</i>. CKG has a complex of multicomponent, multitarget, and multipathway. This study lays the theoretical foundation for further <i>in vitro</i> and <i>in vivo</i> experimental studies and further expands the clinical applications of CKG.

Hao Lv

Jiuxiang Wang

Yujun Zhu

Ting Jiang

Study on the Mechanism of Compound Kidney-Invigorating Granule for Osteoporosis based on Network Pharmacology and Experimental Verification

<i>Objective</i>. Intervertebral disc degeneration (IDD) contributes to cervical and lumbar diseases. Long noncoding RNAs (lncRNAs) are implicated in IDD. This study explored the mechanism of lncRNA HOTAIR in IDD. <i>Methods</i>. Normal and degenerative nucleus pulposus (NP) cells were isolated from NP tissues obtained in intervertebral disc surgery. Cell morphology was observed by immunocytochemistry staining and toluidine blue staining. NP cell markers were detected by RT-qPCR. Proliferation was detected by MTT assay. Autophagy-related proteins were detected by Western blot. Autophagosome was observed by monodansylcadaverine fluorescence staining. Apoptosis was detected by TUNEL staining and flow cytometry. si-HOTAIR and/or miR-148a inhibitor was introduced into degenerative NP cells. Binding relationships among HOTAIR, miR-148a, and PTEN were predicted and verified by dual-luciferase reporter assay and RNA pull-down. Finally, IDD rat models were established. Rat caudal intervertebral discs were assessed by HE staining. Expressions of HOTAIR, miR-148a, and PTEN were determined by RT-qPCR. <i>Results</i>. HOTAIR was highly expressed in degenerative NP cells <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="23.471pt" style="vertical-align:-3.42947pt" id="M1" height="12.7178pt" version="1.1" viewBox="-0.0498162 -9.28833 23.471 12.7178"><g transform="matrix(.013,0,0,-0.013,0,0)"><path id="g113-41" d="M300 -147C201 -63 143 98 143 270S200 602 300 686L282 710C136 610 70 450 70 271V270C70 89 136 -72 282 -170L300 -147Z"/></g><g transform="matrix(.013,0,0,-0.013,4.498,0)"><path id="g113-113" d="M570 304C570 398 525 448 414 448C385 448 343 445 312 434L329 511L321 518C297 504 262 482 244 460L233 411C195 397 159 381 128 358L135 332C160 347 189 360 224 373L111 -147C97 -210 84 -218 17 -231L13 -257L254 -247L259 -218L233 -216C183 -212 177 -202 189 -142L218 -1C238 -10 266 -12 283 -12C351 3 429 48 483 105C543 168 570 242 570 304ZM482 289C482 161 380 33 304 33C278 33 248 51 233 69L303 396C326 400 352 403 369 403C428 403 482 380 482 289Z"/></g><g transform="matrix(.013,0,0,-0.013,15.84,0)"><path id="g117-91" d="M512 -3V55L134 254V256L512 456V514L75 281V230L512 -3Z"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="26.453pt" style="vertical-align:-3.42947pt" height="12.7178pt" version="1.1" viewBox="27.053183800000003 -9.28833 26.453 12.7178"><g transform="matrix(.013,0,0,-0.013,27.103,0)"><path id="g113-49" d="M241 635C89 635 35 457 35 312C35 153 89 -12 240 -12C390 -12 443 166 443 312C443 466 390 635 241 635ZM238 602C329 602 354 454 354 312C354 172 330 22 240 22C152 22 124 173 124 313S148 602 238 602Z"/></g><g transform="matrix(.013,0,0,-0.013,33.343,0)"><path id="g113-47" d="M113 -12C146 -12 170 11 170 46C170 78 146 103 114 103S58 78 58 46C58 11 82 -12 113 -12Z"/></g><g transform="matrix(.013,0,0,-0.013,36.307,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,42.547,0)"><path id="g113-54" d="M153 550H386L412 615L406 623H120L82 318C104 327 142 338 184 338C294 338 347 275 347 187C347 112 305 39 221 39C160 39 119 71 97 89C88 97 80 96 71 90C59 80 50 67 49 57C48 45 52 36 66 23C80 9 123 -12 169 -12C221 -11 288 15 342 59C403 109 431 165 431 225C431 308 366 395 238 395C212 395 165 379 127 364L153 550Z"/></g><g transform="matrix(.013,0,0,-0.013,48.787,0)"><path id="g113-42" d="M275 270C275 450 212 609 64 710L45 686C145 604 203 442 203 270S147 -63 45 -147L64 -170C213 -68 275 89 275 270Z"/></g></svg>.</span></span> si-HOTAIR inhibited degenerative NP cell apoptosis and autophagy <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="23.471pt" style="vertical-align:-3.42947pt" id="M2" height="12.7178pt" version="1.1" viewBox="-0.0498162 -9.28833 23.471 12.7178"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-41"/></g><g transform="matrix(.013,0,0,-0.013,4.498,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,15.84,0)"><use xlink:href="#g117-91"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="26.453pt" style="vertical-align:-3.42947pt" height="12.7178pt" version="1.1" viewBox="27.053183800000003 -9.28833 26.453 12.7178"><g transform="matrix(.013,0,0,-0.013,27.103,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,33.343,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,36.307,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,42.547,0)"><use xlink:href="#g113-54"/></g><g transform="matrix(.013,0,0,-0.013,48.787,0)"><use xlink:href="#g113-42"/></g></svg>.</span></span> HOTAIR upregulated PTEN as a sponge of miR-148a. miR-148a was poorly expressed in degenerative NP cells. miR-148a deficiency partially reversed the inhibition of si-HOTAIR on degenerative NP cell autophagy and apoptosis (all <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M3" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><use xlink:href="#g117-91"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="21.921pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 21.921 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-54"/></g></svg>).</span></span> <i>In vivo</i> assay confirmed that si-HOTAIR impeded autophagy and apoptosis in intervertebral disc tissues, thus improving pathological injury in IDD rats (all <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M4" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><use xlink:href="#g117-91"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="21.921pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 21.921 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-54"/></g></svg>).</span></span> <i>Conclusion</i>. LncRNA HOTAIR promoted NP cell autophagy and apoptosis via promoting PTEN expression as a ceRNA of miR-148a in IDD.

Shujun Zhang

Sheng Song

Wei Cui

Xueguang Liu

Zhenzhong Sun

Mechanism of Long Noncoding RNA HOTAIR in Nucleus Pulposus Cell Autophagy and Apoptosis in Intervertebral Disc Degeneration

In recent years, mindfulness-based interventions (MBIs) are rapidly growing in the workplace. Several meta-analyses conclude that overall MBIs have a moderate effect of alleviating deficit-based experiences, such as burnout and stress, but a small to no effect of promoting asset-based experiences, such as positive affect and well-being. While workplace MBIs vary greatly in their content, format, and duration, the dominant format is still face to face in a group setting, which limits scalability. Our study introduces an emerging workplace intervention called Inner Engineering Online (IEO) and evaluates its effect on reducing stress, burnout, depression, and anxiety and increasing mindfulness and joy. Drawing on the classical yogic science, IEO is a comprehensive web-based multicomponent intervention that utilizes dialectic discourse, meditation, and yogic practices designed to improve physical, mental, and emotional health. Utilizing a randomized active control cross-over experimental design with a sample of 71 employees of an Information Technology company, we tested our hypothesis that IEO training and regular daily yogic practice are likely to lower the stress levels, prevent burnout, and alleviate anxiety and depression, while at the same time promotes positive affect for employees. The results show that IEO program significantly reduces stress only among those who adhere to recommended daily yogic practices. The study is limited by its small sample size. Future research using a large sample is recommended to reexamine the effect of IEO training on occupational health. This trial is registered with <a target="_blank" href="https://clinicaltrials.gov/ct2/show/NCT04126564">NCT04126564</a>.

P. Upadhyay

T. F. H. Chang

S. Hariri

S. Rallabandi

Santha Yathavakilla

V. Novack

B. Subramaniam

The Effect of Inner Engineering Online (IEO) Program on Reducing Stress for Information Technology Professionals: A Randomized Control Study

MicroRNAs (miRNAs) participate in the comprehensive biological process of several cancer types. In our former study, we found that hsa-microRNA- (miR-)28-5p was downregulated, but tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activating protein zeta (14-3-3<i>&#x3b6;</i> or YWHAZ) was upregulated in diffuse large B-cell lymphoma (DLBCL) tissues. We predicted that YWHAZ was a target gene for hsa-miR- 28-5p using bioinformatics analysis. Our goal was to reveal the role of hsa-miR-28-5p in DLBCL. YWHAZ was tested by immunohistochemistry (IHC) in formalin-fixed paraffin-embedded (FFPE) tissues of 137 DLBCL tissues, and the expression of hsa-miR-28-5p and YWHAZ was examined by quantitative real-time polymerase chain reaction (qRT-PCR) in 15 fresh and frozen DLBCL tissues. To study the functional roles of the downregulated hsa-miR-28-5p in DLBCL, a Cell Counting Kit-8 assay was conducted to estimate cell proliferation. Transient transfection of miRNA mimics was performed to overexpress hsa-miR-28-5p, and flow cytometry was performed to examine cell apoptosis and cell cycle progression. A dual-luciferase reporter assay was employed to explore the relationship between hsa-miR-28-5p and YWHAZ. Western blotting and qRT-PCR were used to investigate the function of hsa-miR-28-5p in YWHAZ expression. hsa-miR-28-5p was found to be significantly downregulated in DLBCL tissues and cell lines. Functional studies showed that hsa-miR-28-5p overexpression inhibited cell viability and proliferation, and YWHAZ was predicted to be a target of hsa-miR-28-5p. Dual-luciferase reporter assay, Western blotting, and qRT-PCR verified that hsa-miR-28-5p negatively regulated YWHAZ expression by directly targeting its 3&#x2032; untranslated regions in DLBCL cells. hsa-miR-28-5p may suppress the growth of DLBCL cells by inhibiting YWHAZ expression. These findings could provide novel targets for DLBCL diagnosis and therapy.

Shufang Yan

Yang Chen

Meihong Yang

Qian Zhang

Jiajia Ma

Bo Liu

Liuqing Yang

Xinxia Li

hsa-MicroRNA-28-5p Inhibits Diffuse Large B-Cell Lymphoma Cell Proliferation by Downregulating 14-3-3<i>&#x3b6;</i> Expression

<i>Objective</i>. To explore the main bioactive compounds and investigate the underlying mechanism of Pollen Typhae (PT) against diabetic retinopathy (DR) by network pharmacology and molecular docking analysis. <i>Methods</i>. Bioactive ingredients and the target proteins of PT were obtained from TCMSP, and the related target genes were acquired from the SwissTargetPrediction database. The target genes of DR were obtained from GeneCards, TTD database, DisGeNET database, and DrugBank. The compound-target interaction network was established based on Cytoscape 3.7.2. The protein-protein interaction (PPI) network was constructed via STRING database and Cytoscape 3.7.2. Gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were visualized through DAVID database and Bioinformatics. Ingredient-gene-pathway network analysis was conducted to further screen the ingredients, target proteins, and pathways closely related to the biological mechanism on PT for DR, and molecular docking analysis was performed by SYBYL-X 2.1.1 software. Finally, the mechanism and underlying targets of PT in the treatment of DR were predicted. <i>Results</i>. A total of 8 compounds and 171 intersection targets were obtained based on the online network database. 7 main compounds were screened from compound-target network, and 53 targets including the top six key targets (PTGS2, AKT1, VEGFA, MAPK3, TNF, and EGFR) were further acquired from PPI analysis. The 53 key targets covered 80 signaling pathways, among which PI3K-Akt signaling pathway, focal adhesion, Rap1 signaling pathway, VEGF signaling pathway, and HIF-1 signaling pathway were closely connected with the biological mechanism involved in the alleviation of DR by PT. Ingredient-gene-pathway network shows that AKTI, EGFR, and VEGFA were core genes, kaempferol and isorhamnetin were pivotal ingredients, and VEGF signaling pathway and Rap1 signaling pathway were closely involved in anti-DR. The docking results indicated that five main compounds (arachidonic acid, isorhamnetin, quercetin, kaempferol, and (2R)-5,7-dihydroxy-2-(4-hydroxyphenyl)chroman-4-one) had good binding activity with EGFR and AKT1 targets. <i>Conclusion</i>. The active ingredients in PT may regulate the levels of inflammatory factors, suppress the oxidative stress, and inhibit the proliferation, migration, and invasion of retinal pericytes by acting on PTGS2, AKT1, VEGFA, MAPK3, TNF, and EGFR targets through VEGF signaling pathway, PI3K-Akt signaling pathway, Rap1 signaling pathway, and HIF-1 signaling pathway to play a therapeutic role in diabetic retinopathy.

Rongrong Zhou

De Jin

Yuqing Zhang

Liyun Duan

Yuehong Zhang

Yingying Duan

Xiaomin Kang

Fengmei Lian

Investigating the Mechanisms of Pollen Typhae in the Treatment of Diabetic Retinopathy Based on Network Pharmacology and Molecular Docking

About this journal

<p><em>Evidence-Based Complementary and Alternative Medicine</em> seeks to apply scientific rigor to the study of complementary and alternative medicine, emphasizing on health outcome, while documenting biological mechanisms of action.</p>


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<p>Chief Editor,&nbsp;Jian-Li Gao works as research professorship at the Zhejiang Chinese Medical University, China. Her research focuses on hypertension and oncology, as well as evidence-based use of Traditional Chinese Medicine in reducing the side effects of conventional cancer treatments.&nbsp;</p>


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Evidence-Based Complementary and Alternative Medicine - Table of contents 2022

Evidence-Based Complementary and Alternative Medicine | Hindawi

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Evidence-Based Complementary and Alternative Medicine seeks to apply scientific rigor to the study of complementary and alternative medicine, emphasizing on health outcome, while documenting biological mechanisms of action.

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Evidence-Based Complementary and Alternative Medicine

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