Expression Of Junction Proteins Research Articles

Abstract 3850: Aberrant tumor pericytes in pancreatic ductal adenocarcinoma-a barrier and opportunity for therapeutic advances

Abstract There is a lack of effective treatment for PDAC, often due to abnormal and leaky blood vessels and a lack of proper pericyte coverage, contributing to the inability of the drugs to reach the tumor. We and others showed that pericyte (PC) coverage significantly correlates with vascular integrity, function, and intratumoral hypoxia. However, in PDAC, the PC-endothelial (EC) cell communication is decreased or non-existent, thereby affecting drug delivery and immune function. We propose to re-program tumor-associated pericytes to normalize the tumor blood vessels and revert them to an optimal functional state. We previously showed that tumor-associated pericytes in PDAC exhibit ectopic αSMA expression up to ten times higher than normal pericytes, correlating strongly with vascular instability and hypoxia. Due to significant involvement of αSMA in cellular morphology and structure, tumor-associated pericytes presented biomechanical abnormalities, which diminished intimate association with endothelial cells during tube formation assay. We employed scRNA sequencing to define the pathological signature of tumor-associated pericytes and identify therapeutic targets for vascular normalization. Our analysis revealed considerable heterogeneity in lung pericytes compared to PDAC pericyte clusters, indicating a disrupted vessel hierarchy. Additionally, we identified a distinct pericyte subpopulation characterized by elevated expression of αSMA, MCT1, and gap junction proteins. Alterations in basement membrane gene expression and smooth muscle markers further emphasized the disrupted vascular architecture and impaired pericyte-endothelial cell adhesion within the tumor microenvironment. Our data reveals consistently upregulated monocarboxylate transporters in vascular cells. Therefore, we investigated lactate transporters as a potential target for improving PC-EC adhesion. We have shown that in PDAC, MCT1 lactate exporters are upregulated in EC and PCs. The high amount of lactate produced by PCs decreases the pH in the basement membrane. So, we knocked down MCT1 transporters in PCs to increase basement pH, leading to improved PC-EC attachment and pericyte homeostasis. In conclusion, our study indicates that tumor-associated pericytes undergo phenotype switching and disturbed metabolic communication under the influence of pancreatic cancer cells. These aberrant pericytes might contribute to non-optimal vascular integrity and function. Single-cell RNA sequencing helped understand the molecular signature of the PDAC pericyte, providing a powerful tool to develop novel targeting strategies for vascular normalization. Future work includes exploring the vascular normalization approach by suppressing pericyte phenotype switching to enhance vascular function and chemo- and immunotherapeutic efficacy. Citation Format: Vikneshwari Natarajan, Sangdeuk Ha, Jiha Kim. Aberrant tumor pericytes in pancreatic ductal adenocarcinoma-a barrier and opportunity for therapeutic advances [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 3850.

β-Glucan Extracted from Pichia kudriavzevii DPUL-51-6Y, Kluyveromyces marxianus DPUL-F15, and Saccharomyces cerevisiae DPUL-C6 Shows Ameliorating Effects on DSS-Induced Ulcerative Colitis on BALB/c Mice.

β-Glucans derived from yeast are recognized as beneficial food additives. This study evaluated crude β-glucan extracts from Pichia kudriavzevii DPUL-51-6Y, Kluyveromyces marxianus DPUL-F15, and Saccharomyces cerevisiae DPUL-C6 strains for their anticolitis potential. Chemical analysis revealed that β-glucan was the primary component (71.88-78.47% purity). Notably, the S. cerevisiae extract displayed superior thermal stability and hydration capacity. In RAW264.7 macrophages, β-glucan pretreatment at 100 μg/mL significantly reduced LPS-induced nitric oxide production and pro-inflammatory cytokines by suppressing NF-κB signaling through the reduction of p65 and IκB-α while simultaneously activating the Nrf2 and AHR pathways. In DSS-induced colitis BALB/c mice, oral administration of crude β-glucans alleviated intestinal damage by enhancing tight junction protein expression and restoring gut microbiota composition, characterized by an increased abundance of Lactobacillus and Prevotella. These effects were correlated with the increased production of microbial metabolites, including indole-3-lactic acid, indole-3-β-acrylic acid, tryptophol, and short-chain fatty acids (acetic, propionic, and butyric acids). Mechanistically, β-glucan mitigated colitis through the dual activation of Nrf2/AHR pathways and the inhibition of NF-κB. This study suggests that yeast-derived β-glucan plays a significant role in mitigating the inflammatory response and may alleviate ulcerative colitis by reshaping the microbial community and metabolite profiles in the host intestinal tract.

Parental high-fat diet induces upregulation of macrophage receptor with collagenous structure expression and exacerbates colorectal inflammation via the nuclear factor kappa-B pathway in offspring.

Parental high-fat diet induces upregulation of macrophage receptor with collagenous structure expression and exacerbates colorectal inflammation via the nuclear factor kappa-B pathway in offspring.

HIV-associated penile anaerobes disrupt epithelial barrier integrity.

Specific anaerobic taxa within the penile microbiome-the Bacteria Associated with Seroconversion, Inflammation and Immune Cells (BASIC) species-enhance HIV-1 susceptibility, in part by recruiting susceptible cells to the inner foreskin. However, their effect on epithelial barrier integrity has not been described. Using foreskin tissues and penile swabs from 116 males undergoing voluntary medical male circumcision, we assessed the relationship between BASIC species and foreskin epithelial thickness, junction protein expression, and cellular proliferation. The absolute abundance of BASIC species was associated with reduced tissue expression of the epithelial junction proteins claudin-1 and E-cadherin, and with elevated soluble E-cadherin in penile secretions, suggesting proteolytic cleavage. These effects were not seen in participants with a high abundance of control taxa without high levels of BASIC species. The BASIC species Prevotella bivia, but not Peptostreptococcus anaerobius or Dialister micraerophilus, was shown to directly degrade recombinant human E-cadherin and to increase the release of soluble E-cadherin from foreskin epithelial cells in vitro. In vivo BASIC species absolute abundance was also linked to a thicker nucleated epithelium and increased keratinocyte proliferation, with no change in stratum corneum thickness. Therefore, BASIC species may enhance penile HIV susceptibility by directly disrupting epithelial integrity, in addition to previously described target cell recruitment.

Impact of maternal Lactiplantibacillus plantarum S58 supplementation on offspring rat immunity and gut health.

Pregnancy and lactation provide several opportunities for maternal dietary interventions to confer health benefits to newborns. However, the effects of maternal probiotic supplementation during pregnancy and lactation on offspring immunity and intestinal health remain largely unknown. This study aimed to investigate the effects of supplementation with the probiotic Lactiplantibacillus plantarum S58 (LP.S58) during pregnancy and lactation on the intestinal health and immunity of rat offspring. The results demonstrated that LP.S58 was effectively transmitted to the gastrointestinal tissues of offspring rats following maternal supplementation during pregnancy, lactation, or both, without affecting the normal development of individual organs. Furthermore, maternal LP.S58 supplementation significantly increased the serum levels of IL-4, IL-10, SOD, and T-AOC, while reducing those of TNF-α, IL-1β, IL-6, LPS, and NOS in the offspring. Additionally, it upregulated the mRNA expression of tight junction proteins and downregulated pro-inflammatory factors in the offspring rats, thereby improving intestinal health. More importantly, LP.S58 supplementation significantly increased the levels of beneficial gut bacteria, including Akkermansia and Lactobacillus, in the offspring rats. In conclusion, these findings indicate that maternal supplementation with specific probiotics during pregnancy and lactation may positively influence the immune function and intestinal development of offspring.

Ebola Virus Glycoprotein Impairs Human Retinal Pigment Epithelial Barrier Function via the PI3K/Akt-Nrf2 Pathway.

Ebola virus (EBOV) causes deadly Ebola virus disease (EVD), and EVD survivors are at high risk of developing blinding ocular complications, which associate with the breakdown of human retinal pigment epithelial (RPE) barrier. Here, we demonstrated EBOV glycoprotein (GP) could directly impair RPE barrier function. EBOV GP significantly decreased expression of tight junction (TJ) proteins in RPE monolayers, resulting in an increase of monolayer permeability. EBOV GP activated PI3K/Akt pathway and induced oxidative stress in RPE cells as evidenced by an increase in the production of reactive oxygen species (ROS), decreased expression of an antioxidant factor, nuclear factor erythroid 2-related factor 2 (Nrf2), and its downstream proteins heme oxygenase 1 (HO-1) and NAD(P)H dehydrogenase (quinone) 1 (NQO1). We found activating Nrf2 could counteract EBOV GP-induced RPE barrier injury. Furthermore, GP2 subunit is the key region in the GP that impairs RPE barrier function. Destruction of RPE barrier function by EBOV GP leads to translocation of bacteria and HIV-1. We confirmed EBOV GP-mediated impairment of RPE barrier function in mice. As an Nrf2 activator, resveratrol displays protective effects on the RPE barrier function. Collectively, our study demonstrates EBOV GP impairs the RPE barrier function through PI3K/Akt-Nrf2 pathway and resveratrol is a promising therapeutic agent for EVD-associated retinal complications.

Irisin mitigates osteoporotic-associated bone loss and gut dysbiosis in ovariectomized mice by modulating microbiota, metabolites, and intestinal barrier integrity

BackgroundOsteoporotic bone defects significantly affect patient health and quality of life. The gut-bone axis plays a crucial role in osteoporosis, and disruptions in gut microbiota are linked to systemic inflammation and compromised bone metabolism. Irisin, a myokine, has shown potential in protecting against osteoporosis, but its mechanisms of action on the gut-bone axis remain unclear. This study aimed to investigate the role of irisin in mitigating osteoporotic bone defects by examining its effects on gut microbiota, related metabolites, and intestinal barrier integrity.MethodsAn osteoporosis model was created using ovariectomized (OVX) mice. The mice were divided into Sham, OVX, and r-irisin groups. Mice in the r-irisin group received intraperitoneal injections of 100 μg/kg irisin twice weekly for five weeks. Bone parameters were analyzed by micro-CT and histological staining. Gut microbiota composition was examined via 16S rDNA sequencing. Intestinal cytokines and barrier proteins were measured using immunohistochemistry and ELISA. Fecal metabolomic profiling was conducted using liquid chromatography-tandem mass spectrometry (LC–MS/MS), and correlations between gut microbiota, metabolites, and bone metabolism markers were evaluated.ResultsIrisin treatment improved bone mineral density (BMD), bone volume/tissue volume (BV/TV), trabecular bone thickness (Tb.Th), and trabecular number (Tb.N), and reduced trabecular separation (Tb.Sp) in OVX mice. It enhanced new bone formation and collagen deposition. Irisin restored intestinal barrier integrity by increasing tight junction protein expression and reducing inflammatory cytokines in intestinal tissues. It also modulated gut microbiota diversity, reducing Firmicutes and increasing Verrucomicrobiota abundance. Key fecal metabolites, including atractylon (r = − 0.60, P < 0.01) and enterodiol (r = + 0.83, P < 0.01), showed strong correlations with BMD.ConclusionIrisin mitigates osteoporotic bone defects by enhancing bone formation, restoring intestinal barrier integrity, modulating gut microbiota composition, and influencing fecal metabolites. These preclinical findings highlight irisin’s potential to mitigate osteoporosis via the gut-bone axis.

Iturin A Potentiates Differentiation of Intestinal Epithelial Defense Cells by Modulating Keap1/Nrf2 Signaling to Mitigate Oxidative Damage Induced by Heat-Stable Enterotoxin B

Intestinal stem cells (ISCs) maintain epithelial renewal through their proliferation and differentiation capabilities, responding to various intestinal insults. However, the impact of iturin A, a natural antimicrobial peptide, on ISC viability and its potential to mitigate heat-stable enterotoxin b (STb)-induced intestinal damage remains unclear. Our recent study demonstrated that oral administration of iturin A enhances tight junction protein expression, accelerates crypt-villus regeneration, and restores epithelial barrier integrity in STb-exposed mice. Furthermore, iturin A promotes ISC proliferation and differentiation, significantly increasing the numbers of goblet and Paneth cells in the jejunum following STb exposure. Notably, iturin A regulates intestinal homeostasis by scavenging reactive oxygen species (ROS), while elevating total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) levels in both serum and jejunal mucosa. Mechanistically, iturin A facilitates nuclear factor-erythroid 2- related factor 2 (Nrf2) release by disrupting Kelch-like ECH-associated protein 1 (Keap1), leading to the upregulation of the antioxidant enzyme glutathione peroxidase 4 (GPX4). In conclusion, our findings indicate that iturin A alleviates oxidative stress induced by STb through modulation of the Keap1/Nrf2 pathway and promotes ISC differentiation into goblet and Paneth cells, thereby enhancing resistance to STb-induced damage.

Six Weeks of Moderate-Intensity Treadmill Exercise Improves Intestinal Barrier and Intestinal Inflammation in Parkinson's Disease Mice.

More than 80% of patients with Parkinson's disease (PD) exhibit severe gastrointestinal symptoms, which seriously affect life quality of life. Several large-scale epidemiological studies have confirmed that exercise can improve motor symptoms of PD patients, but the influence on gastrointestinal symptoms has not been reported. To clarify whether exercise can enhance intestinal barrier and ameliorate intestinal inflammation in PD mice, we examined whether moderate-intensity treadmill exercise for 6weeks could alleviate gastrointestinal symptoms in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced subacute PD mice. Our results demonstrated that 6weeks moderate-intensity treadmill exercise enhanced the expression of Muc-2 and tight junction proteins, while reducing the expression of cytokines and chemokines, in the distal colon. Moreover, 6weeks of treadmill exercise reduced the concentrations of short-chain fatty acids (SCFAs) and the expression of G protein-coupled receptor 43 (GPR43) to maintain the intestinal barrier and alleviate intestinal inflammation. Further data showed that 6weeks of moderate-intensity treadmill exercise enhanced insulin-like growth factor 1 (IGF-1) expression and activated the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Taken as a whole, these results revealed that 6weeks of moderate-intensity treadmill exercise enhanced intestinal barrier function, reduced intestinal inflammation and corrected abnormal concentrations of SCFAs by activating IGF-1/PI3K/Akt pathway in MPTP-induced subacute PD mice.

HFD-induced LPS translocation and elevated blood lipids exacerbated the inflammatory response in allergic rhinitis

Allergic rhinitis (AR) is one of the most prevalent chronic diseases, with studies indicating that a high-fat diet (HFD) may heighten susceptibility to AR. This study aims to investigate the impact of HFD on ovalbumin (OVA)-induced AR using both an OVA-sensitized rat model and a macrophage model treated with palmitic acid (PA). The systemic effects of HFD were explored with respect to intestinal barrier integrity, serum lipids and lipopolysaccharide (LPS) levels, and inflammatory response. In AR rats fed with HFD, there was a reduction in the expression of tight junction proteins in colon tissues, increased serum levels of lipids and LPS, and elevated inflammatory responses in both nasal lavage fluid (NLF) and serum. Additionally, there was enhanced NF-κB and NLRP3 inflammasome activity observed in both nasal and colon tissues. In vitro experiments demonstrated that PA and LPS synergistically amplified inflammatory responses in THP-1-derived macrophages, paralleling the systemic findings. These results suggest that HFD-induced intestinal barrier dysfunction facilitates the translocation of LPS into the bloodstream. Elevated serum LPS level, together with increased blood lipids levels, may exacerbate the inflammatory response in AR through the activation of NF-κB and NLRP3 inflammasome.

AhR Activation at the Air-Blood Barrier Alters Systemic microRNA Release After Inhalation of Particulate Matter Containing Environmentally Persistent Free Radicals.

Particulate matter containing environmentally persistent free radicals (EPFRs) is formed when organic pollutants are incompletely burned and adsorb to the surface of particles containing redox-active metals. Our prior studies showed that in mice, EPFR inhalation impaired vascular relaxation in a dose- and endothelium-dependent manner. We also observed that activation of the aryl hydrocarbon receptor (AhR) in the alveolar type-II (AT-II) cells that form the air-blood interface stimulates the release of systemic factors that promote endothelial dysfunction in vessels peripheral to the lung. AhR is a recognized regulator of microRNA (miRNA) biogenesis, and miRNA control diverse signaling pathways. We thus hypothesized that systemic EPFR-induced vascular endothelial dysfunction is initiated via AhR activation in AT-II cells, resulting in a systemic release of miRNA. Using a combustion reactor, we generated EPFR of two free radical concentrations-EPFRlo (1016-17 radicals/g particles) and EPFR (1018-19 radicals/g)-and exposed mice by inhalation. EFPR inhalation resulted in changes in a distinct array of miRNA in the plasma, and these miRNAs are linked to multiple systemic effects, including cardiovascular diseases and dysregulation of cellular and molecular pathways associated with cardiovascular dysfunction. We identified 17 miRNA in plasma that were altered dependent upon both AhR activation in AT-II cells and ~ 280ug/m3 EPFR exposure. Using Ingenuity Pathway Analysis, we found that 5 of these miRNAs have roles in modulating endothelin-1 and endothelial nitric oxide signaling, known regulators of endothelial function. Furthermore, EPFR exposure reduced the expression of lung adherens and gap junction proteins in control mice but not AT-II-AhR deficient mice, and reductions in barrier function may facilitate miRNA release from the lungs. In summary, our findings support that miRNA may be systemic mediators promoting endothelial dysfunction mediated via EPFR-induced AhR activation at the air-blood interface.

Effects of co-exposure to microplastics and perfluorooctanoic acid on the Caco-2 cells.

Effects of co-exposure to microplastics and perfluorooctanoic acid on the Caco-2 cells.

Current Approaches and Future Directions for the Treatment of Solid Tumour Brain Metastases

Brain metastases (BrM) are most common among patients with metastatic lung cancer, breast cancer, and melanoma. Historically, management of BrM consisted of local treatments with surgical resection and/or radiation therapy, with either whole brain radiation therapy (WBRT) or stereotactic radiosurgery (SRS). Current guidelines recommend SRS as the initial therapy for patients who have up to four BrM, but several studies have demonstrated that upfront SRS may be considered for some patients who have more than four BrM given additional clinical benefits of improved memory function and quality of life compared to WBRT. Systemic therapies are increasingly understood to cross the blood-brain barrier (BBB) following disruption of its integrity upon BrM development. Disseminated tumour cells intravasate into the circulation and spread hematogenously with a “seed and soil” tropism for the brain that provides a suitable tumour microenvironment. Tumour cells extravasate and increase the permeability of the BBB by decreasing tight junction protein expression, decreasing astrocyte pedicles, reducing pericyte coverage, and increasing neoangiogenesis. The altered integrity of the BBB allows penetration of large drug molecules, such as antibody-drug conjugates (ADCs), which exert their therapeutic effects on BrM by binding to tumour cell-specific epitopes and releasing a cytotoxic payload, even in the absence of radiation. Other therapeutic mechanisms of action include molecular (passive or receptor-mediated transport), physical (radiation or focused ultrasound), direct delivery to the brain (intrathecal or intratumoral), and cell‑mediated (immune cell extravasation) (Figure 1).

Protective effect of Stropharia rugosoannulata polysaccharide and its derivatives on dextran sodium sulfate-induced colitis

Abstract Ulcerative colitis is a common inflammatory bowel disease. This study evaluated the protective effect and potential mechanism of Stropharia rugosoannulata polysaccharide (SP-1a) and its carboxymethylated and phosphorylated derivatives (CSP-1a and PSP-1a) against dextran sulfate sodium (DSS)-induced ulcerative colitis. The results showed that treatment with SP-1a and its derivatives alleviated the symptoms of weight loss, colon shortening, and blood in the stool induced by . SP-1a and its derivatives restore the integrity of the intestinal barrier by controlling the expression of tight junction proteins. Furthermore, they play an anti-inflammatory role by reducing oxidative stress and inhibiting the expression of pro-inflammatory factors, pro-inflammatory proteins, and nuclear factor kappa-B (NF-κB) signaling pathways. The anti-inflammatory effects of CSP-1a and PSP-1a were greater than those of SP-1a. These results indicate that SP-1a could be a potential natural medicine to protect against DSS-induced colitis.

Yeast β-glucan alleviates the subacute rumen acidosis-induced mitochondrial dysfunction and cell structure integrity injury in yak rumen epithelial cells via the TLR2/PI3K/mTOR signaling pathway.

Yeast β-glucan alleviates the subacute rumen acidosis-induced mitochondrial dysfunction and cell structure integrity injury in yak rumen epithelial cells via the TLR2/PI3K/mTOR signaling pathway.

3'-Sialyllactose and B. infantis synergistically alleviate gut inflammation and barrier dysfunction by enriching cross-feeding bacteria for short-chain fatty acid biosynthesis

ABSTRACT Ulcerative colitis (UC) poses significant threats to human health and quality of life worldwide, as it is a chronic inflammatory bowel disease. 3'-sialyllactose (3'−SL) is a key functional component of milk oligosaccharides. This study systematically evaluates the prebiotic effects of 3'-SL and its therapeutic potential in combination with Bifidobacterium infantis (B. infantis) for UC. The findings reveal that 3'-SL and B. infantis synergistically mitigate intestinal inflammation and barrier dysfunction by promoting the production of short-chain fatty acids (SCFAs) through cross-feeding mechanisms among gut microbiota. Individually, 3'-SL, B. infantis, and the synbiotic treatment all effectively alleviated UC symptoms, including reduced weight loss, improved disease activity scores, and prevention of colon shortening. Histopathological and immunofluorescence analyses further demonstrated that the synbiotic treatment significantly ameliorated colonic injury, enhanced barrier function, restored goblet cell counts, increased glycoprotein content in crypt goblet cells, and upregulated the expression of tight junction proteins (ZO-1, occludin, and claudin-1). Notably, the synbiotic treatment outperformed the individual components by better restoring gut microbiota balance, elevating SCFA levels, and modulating serum cytokine profiles, thereby reducing inflammation. These findings provide mechanistic insights into the protective effects of the synbiotic and underscore its therapeutic potential for UC and other intestinal inflammatory disorders.

Chrysophanol Attenuates Cardiac Fibrosis and Arrhythmia by Suppressing the Endoplasmic Reticulum Stress/Pyroptosis Axis and Inflammation

ABSTRACTChrysophanol (CHR), one of the principal bioactive compounds extracted from the rhizome of Rheum palmatum L., is known for its anti‐inflammatory, antioxidative, anti‐cancer, and cardioprotective effects. However, the effect of CHR on cardiac fibrosis remains elusive. In this study, mice were administered isoproterenol (ISO) to induce cardiac fibrosis in vivo, and cardiac fibroblasts were pretreated with transforming growth factor‐β1 (TGF‐β1) to induce the transformation of fibroblasts into myofibroblasts in vitro. Western blot and reverse transcription‐quantitative polymerase chain reaction analyses were performed to evaluate the endoplasmic reticulum (ER) stress and pyroptosis. Immunohistochemistry staining and ELISA analyses were used to detect the inflammation level. In vivo electrophysiological studies were conducted to assess arrhythmia susceptibility. Our findings revealed that CHR treatment ameliorated cardiac dysfunction and fibrosis in ISO‐challenged mice. Moreover, CHR reduced susceptibility to ventricular fibrillation by reducing ventricular electrical remodeling and increasing the expression of gap junction proteins and ion channels. Additionally, CHR inhibited the TGF‐β1‐stimulated transformation of cardiac fibroblasts into myofibroblasts in vitro. CHR inhibited ER stress, pyroptosis, and inflammation in vivo and in vitro. Furthermore, tunicamycin (TM)‐induced activation of ER stress abolished the protective effects of CHR. CHR treatment attenuates cardiac fibrosis and arrhythmia by suppressing the ER stress/pyroptosis axis and inflammation.

Edgeworthia gardneri (Wall.) Meisn protects against HFD-induced murine atherosclerosis through improving gut microbiota-mediated intestinal barrier integrity.

Edgeworthia gardneri (Wall.) Meisn protects against HFD-induced murine atherosclerosis through improving gut microbiota-mediated intestinal barrier integrity.

Zinc Glycine supplementation improves bone quality in meat geese by modulating gut microbiota, SCFA's, and gut barrier function through Wnt10b/NF-κB axis.

Zinc Glycine supplementation improves bone quality in meat geese by modulating gut microbiota, SCFA's, and gut barrier function through Wnt10b/NF-κB axis.

Elucidating the mechanism of the first Chinese herbal formula Shuangxia Decoction to alleviate insomnia using multi-omics technologies.

Elucidating the mechanism of the first Chinese herbal formula Shuangxia Decoction to alleviate insomnia using multi-omics technologies.