Effects Of Baicalin Research Articles

PSVIII-26 Baicalin Alleviates Lincomycin-Induced Intestinal Injury By Regulating Gut Microbiota in Weaned Pigs

Abstract Lincomycin and related antibiotics are widely used in swine clinics, but its side effects including diarrhea and inflammatory bowel disease are difficult to detect and controlled. The purpose of this study was to investigate the effect and mechanism of baicalin, a flavonoid extracted from scutellaria baicalensis, on alleviating lincomycin-related intestinal injury. Forty-eight 21-day-old weaned pigs were selected and randomly divided into three groups: control group, lincomycin group (LC), and baicalin treatment group (LC + BL). Pigs in the LC and LC + BL groups were administered with 1 g/kg lincomycin in feed for 1 week. In the second week, pigs in the LC + BL group were administered 500 mg/kg baicalin in feed. After 2 weeks, 6 piglets in each group were selected to obtain intestinal samples for subsequent analysis, and the body weight of the remaining piglets was recorded on day 28. The results showed that lincomycin significantly reduced the body weight of the pigs on day 28 (P < 0.05), but baicalin treatment restored the body weight of piglets on day 28 to the control level. As for intestinal morphology, lincomycin damaged intestinal morphology and reduced villus height in the jejunum of piglets, but these indexes recovered to the control level after baicalin treatment (P < 0.05). In addition, lincomycin decreased claudin-1, TNF-α, and IL-1β mRNA expression in the jejunum (P < 0.05), but these indexes recovered to the control level after baicalin treatment. Then 16S rDNA sequencing was used to examine the microbial composition in the jejunum. Lincomycin significantly increased the abundance of Proteobacteria, Chloroflexi, and Deinococcota (P < 0.05), but baicalin decreased the abundance of Chloroflexi, Acidobacteriota, Patescibacteria, Myxococcota, and Gemmatimonadota in phylum level (P < 0.05). At genus level, lincomycin significantly increased the abundance of Citrobacter, Corynebacterium, Delftia, Agathobacter, Trichococcus, Tissierellales, Enterococcus, Paracoccus, Shewanella, unclassified_c__Clostridia, Alistipes, Sphingomonas, and Massilia, etc (P < 0.05). However, these results were not observed in the LC + BL group, and baicalin treatment increased the abundance of beneficial bacteria such as norank_f__Muribaculaceae (P < 0.05). Fecal microbiota transplantation was employed to further investigate whether these results were relevant to gut microbes. The body weight, villus height, and crypt depth of mice receiving LC group microbiota were significantly lessthan that of the control group, while the body weight of mice receiving LC + BL group microbiota was not significantly different from that of the control group. Overall, these results suggest that baicalin may alleviate lincomycin-induced intestinal damage and inflammation by inhibiting the growth of harmful bacteria. Our findings expand our knowledge of antibiotic-induced injury and provide new avenues for identifying potential therapeutic targets for the treatment of antibiotic-induced injury and its complications.

Protective effects of baicalin on diethyl nitrosamine-induced liver cirrhosis by suppressing oxidative stress and inflammation.

Baicalin (BA) is a natural product extract with anti-inflammatory, antioxidant, and hepatoprotective properties. Given that the exact underlying mechanisms responsible for the impact of BA on liver cirrhosis remain ambiguous, a detailed investigation is sorely needed. Accordingly, a rat liver cirrhosis model was established via the intraperitoneal injection of diethyl nitrosamine (DEN, 100 mg/kg). Following the modeling, these rats were given BA (100 mg/kg) or N-acetylcysteine (NAC, 150 mg/kg) alone or in combination. The pathological morphology of rat liver tissues in each group was observed by hematoxylin and eosin staining and Masson's trichrome staining. The expression of fibrosis-related proteins was evaluated by Western blot, and the levels of liver function-related biochemical indexes, oxidative stress-related indexes, and inflammatory factors in the serum by enzyme-linked immunosorbent assays (ELISA). The level of mitochondrial reactive oxygen species was measured by flow cytometry. The results depicted that in the rat model of DEN-induced liver cirrhosis, BA reduced the expression of fibrosis-related proteins (collagen type I alpha 1, α-smooth muscle actin, and transforming growth factor-β1), thereby alleviating the structural fibrosis of liver tissue. Furthermore, BA could diminish the level of mitochondrial reactive oxygen species, and the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), and monocyte chemotactic protein-1 (MCP-1), while promoting albumin, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels. Notably, all these effects of BA above were strengthened following the combined treatment of BA and NAC. On the whole, BA suppresses liver fibrosis by inhibiting oxidative stress and inflammation, thereby exerting a hepatoprotective effect.

MicroRNA-124a regulates the differentiation of bone marrow mesenchymal stem cells into neurons

Objective This study investigated the effects of microRNA-124a on the differentiation of bone marrow mesenchymal stem cells (BMSCs) and its underlying mechanism. Methods Flow cytometry was used for isolation and identification of BMSCs. Real-time polymerase chain reaction (RT-PCR) was used to detect gene mRNA expression. Apoptosis was detected using Annexin V-FITC/PI Apoptosis Detection Kit. Cell proliferation ability was tested using Cell Counting Kit-8 (CCK-8). The differentiation of BMSCs into neuron inducers β-thiol ethanol or baicalin formed the basis of the study. Results β-thiol ethanol markedly suppressed the microRNA-124a expression of BMSCs, baicalin markedly induced the microRNA-124a expression of BMSCs and β-thiol ethanol or baicalin promoted apoptosis and reduced the growth of BMSCs. Only the microRNA-124a inhibitor did not affect apoptosis or the differentiation of BMSCs, and it increased the effects of β-thiol ethanol or baicalin on the apoptosis of BMSCs. Conclusion β-thiol ethanol and baicalin treatment could affect microRNA-124a expression in BMSCs. We demonstrated that microRNA-124a promoted the differentiation of BMSCs into neurons.

Retracted] Protective effects of baicalin on rabbit articular chondrocytes invitro.

[This retracts the article DOI: 10.3892/etm.2017.4116.].

Widely targeted metabolomics unveils baicalin-induced hippocampal metabolic alternations in a rat model of chronic unpredictable mild stress

Baicalin has various neuroprotective effects in models of nervous system disease. Our study has shown baicalin could alleviate depressive-like behaviors in a neuroendocrine mouse model. But the systematic metabolic characteristic and particular targets of baicalin in regulating depressive behaviors have never been investigated. Therefore, this study aims to reveal the hippocampal metabolic profiling of chronic unpredictable mild stress (CUMS) induced depressive rats and the potential metabolic variations after baicalin treatment. We first used the sucrose preference test and open field test to access the antidepressant effects of baicalin. Then, metabolites of the hippocampus after baicalin therapy were monitored by widely-targeted metabolomics based on ultra-performance liquid chromatography-tandem mass spectrometry technology. Finally, the potential mechanism associated with neurogenesis obtained from metabolomics was verified by immunohistochemistry. The results showed that baicalin(40,80 mg/kg) could significantly alleviate depressive behaviors induced by CUMS as demonstrated by an increase in sucrose preference and movement distance and stand-up times in open field test. In the metabolomic analysis, a total of 733 metabolites were identified after baicalin treatment including 15 differential metabolites such as organic acid and its derivatives, heterocyclic compounds, fatty acid, bile acids, amino acid and its metabolites, and so on. Enrichment for differential metabolites showed that the differential metabolites might be involved in the process of folate and cofactor biosynthesis, cholesterol metabolism, primary bile acid biosynthesis, tyrosine metabolism and dopaminergic synapse. Moreover, immunohistochemical analysis confirmed baicalin could facilitate hippocampal neurogenesis of depressive rats in CUMS model. These results suggested baicalin might exert antidepressant effects through regulating the differential metabolites which might play a crucial role in inhibiting oxidative stress and improving neurogenesis. Our findings wish to discover the potential mechanism of baicalin on depression from the metabolomics perspective and promote its clinical application.

The anti-inflammatory and autophagy-induced effects of baicalin in ankylosing spondylitis hip ligament fibroblasts

IntroductionAnkylosing spondylitis (AS) is characterised by chronic inflammation that affects the axial skeleton and peripheral joints. Hip involvement occurs in nearly one-third of patients with AS and is considered a poor prognostic sign. Inflammation is also associated with AS progression. Baicalin is a bioactive flavonoid possessing both anti-inflammatory and antioxidant properties, although its activity in AS has not been investigated. The aim of our study was to evaluate the effects of baicalin on AS pathogenesis-related cells and investigate the potential mechanisms. MethodsFibroblasts were isolated from AS patients who met the modified New York criteria and underwent total hip arthroplasty. Flow cytometry was used to identify the fibroblasts. Cytokine expression was evaluated by enzyme-linked immunosorbent assay and real-time polymerase chain reaction, and protein expression was detected using western blotting. Immunofluorescence and transmission electron microscopy were used to assess autophagy. ResultsBaicalin effectively inhibited the expression of inflammatory cytokines upregulated by lipopolysaccharides in AS hip ligament fibroblasts. Moreover, the lipopolysaccharide-triggered nuclear factor kappa-B (NF-κB) and Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling pathways were also suppressed by baicalin. Furthermore, baicalin markedly induced autophagy, which suppressed inflammation dose-dependently. ConclusionsThe anti-inflammatory activity of baicalin was mediated by the repression of NF-κB and JAK/STAT signalling pathways. Furthermore, the induction of autophagy may contribute to inhibiting inflammation.

Hippocampus protection from apoptosis by Baicalin in a LiCl-pilocarpine-induced rat status epilepticus model through autophagy activation.

Autophagy is associated with hippocampal injury following status epilepticus (SE) and is considered a potential therapeutic mechanism. Baicalin, an emerging multitherapeutic drug, has shown neuroprotective effects in patients with nervous system diseases due to its antioxidant properties. To investigate the potential role of autophagy in LiCl-pilocarpine-induced SE. The drugs were administered 30 min before SE. Nissl staining showed that Baicalin attenuated hippocampal injury and reduced neuronal death in the hippocampus. Western blotting and terminal deoxynucleotidyl transferase dUTP nick end labeling assay confirmed that Baicalin reversed the expression intensity of cleaved caspase-3 and apoptosis in hippocampal CA1 following SE. Fur-thermore, western blotting and immunofluorescence staining were used to measure the expression of autophagy markers (p62/SQSTM1, Beclin 1, and LC3) and apoptotic pathway markers (cleaved caspase-3 and Bcl-2). Baicalin significantly upregulated autophagic activity and downregulated mitochondrial apoptotic pathway markers. Conversely, 3-methyladenine, a commonly used autophagy inhibitor, was simultaneously administered to inhibit the Baicalin-induced autophagy, abrogating the protective effect of Baicalin on the mitochondrial apoptotic level. We illustrated that Baicalin-induced activation of autophagy alleviates apoptotic death and protects the hippocampus of SE rats.

Baicalin: A potential therapeutic agent for diabetes and renal protection

Background: Diabetes is a complex metabolic disease manifested by raised glucose levels in the blood and impaired insulin function leading to various organ complications, including diabetic nephropathy. Baicalin, a flavonoid derived from Scutellaria baicalensis Georgi, has garnered substantial attention for its diverse beneficial effects, including anti-inflammatory, anti-allergic, anti- apoptotic properties, etc. Intriguingly, in vivo studies in rats have further unveiled baicalin’s potential to directly modulate pancreatic beta cells, suggesting a promising role as an anti-diabetic agent.Objective: The purpose of this study is to comprehensively explore the anti-diabetic effect of baicalin, focusing on key parameters such as plasma insulin levels, glucose levels, hemoglobin, and glycated hemoglobin levels in streptozotocin-induced diabetic rats. Additionally, we sought to explore Baicalin’s ability to provide renal protection by evaluating serum renal markers. Methodology: This study involved a total of 30 Wistar albino male rats. Diabetes was created in rats by a single intraperitoneal streptozotocin injection (40 mg/kg). After 72 hours, the rats with diabetes were segregated into four treatment groups (Group II to Group V) comprising 6 animals each. Group I consists of six normal control rats (without diabetes). The groups received different treatment protocols, including normal saline, DMSO, Baicalin (50 mg/kg/day), and glibenclamide (6 mg/kg/day) for 45 days. Throughout the study, meticulous observations were made regarding the animals’ general appearance, body weight, behavior, and their fasting glucose levels in venous blood.Results: Oral dosing with Baicalin at the rate of 50 mg/kg body weight revealed notable enhancements in insulin secretion and hemoglobin levels, alongside notable reductions in blood levels of glucose and glycated hemoglobin compared to the glibenclamide-treated type 2 diabetic rats. Additionally, Baicalin displayed a protective action on renal tissue, as shown by reduced serum creatinine, uric acid, and urea levels.Conclusion: Our investigation unveils Baicalin’s potential as a promising anti-diabetic agent with the added benefit of renal tissue protection. The observed improvements in various physiological parameters warrant further exploration of Baicalin’s therapeutic mechanisms and clinical applications, presenting it as a compelling candidate for diabetes management and diabetic nephropathy prevention. IAEC Approval No: AVMC/IAEC/2019/07/25/08 Keywords: Baicalin, Blood glucose, Diabetes, Male wistar rats, Streptozotocin

Therapeutic Effects of Baicalin on Diseases Related to Gut-Brain Axis Dysfunctions.

The gut-brain axis is an active area of research. Several representative diseases, including central nervous system disorders (Alzheimer's disease, Parkinson's disease, and depression), metabolic disorders (obesity-related diseases), and intestinal disorders (inflammatory bowel disease and dysbiosis), are associated with the dysfunctional gut-brain axis. Baicalin, a bioactive flavonoid extracted from Scutellaria baicalensis, is reported to exert various pharmacological effects. This narrative review summarizes the molecular mechanisms and potential targets of baicalin in disorders of the gut-brain axis. Baicalin protects the central nervous system through anti-neuroinflammatory and anti-neuronal apoptotic effects, suppresses obesity through anti-inflammatory and antioxidant effects, and alleviates intestinal disorders through regulatory effects on intestinal microorganisms and short-chain fatty acid production. The bioactivities of baicalin are mediated through the gut-brain axis. This review comprehensively summarizes the regulatory role of baicalin in gut-brain axis disorders, laying a foundation for future research, although further confirmatory basic research is required.

An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model.

Baicalin has been shown to promote spatial learning and neural regeneration, which might increase the differentiation of neural stem cells in Alzheimer's disease (AD) rat models. We aimed to study the role of baicalin on neuronal pentraxin-1 (NPTX-1), neuronal pentraxin-2 (NPTX-2), and C-reactive protein (CRP) in AD model rats. The 30 male Sprague Dawley rats were divided into three groups: the control group, the AD model group, and the AD + baicalin group. Then, the Morris water maze was used to verify the effect of baicalin on the memory and spatial learning of rats. Immunohistochemistry and immunofluorescence were used to observe the expression of NPTX-1, NPTX-2, and CRP in brain tissue. Compared with the AD model group, the AD rats treated with baicalin spent significantly less time finding escape latencies (P = 0.008) and had longer cross-platform times in the target quadrant (P = 0.015). In addition, the AD + baicalin group had significantly higher numbers of hippocampal neurons compared with the AD model group (P < 0.05). Baicalin also obviously decreased the apoptosis of neurons. Moreover, compared with the AD model group, the NPTX-1 and CRP expression in the AD + baicalin group was significantly reduced (P = 0.000) while the expression of NPTX-2 in the brain tissue of AD rats was significantly increased (P = 0.000). Baicalin can play a therapeutic role by downregulating NPTX-1, upregulating NPTX-2, and downregulating CPR in AD model rats.

Baicalin Relieves Airway Inflammation in COPD by Inhibiting miR-125a.

To investigate the effects of Baicalin on the apoptosis of human bronchial epithelial cells (16HBE) induced by cigarette smoke extract (CSE) and the release of inflammatory factors, and to clarify its possible mechanism. CSE was used to treat 16HBE cells and construct COPD cell model. The activity of 16HBE cells was detected by CCK-8 and BrdU. Real-time fluorescence quantitative PCR (RT-QPCR) was used to detect the expression level of miR-125a in each group of 16HBE cells. At the same time, the levels of 16HBE inflammatory cytokines IL-1β, IL-8, IL-6, and TNF-α were detected. The apoptosis rate of 16HBE cells in each group was detected by TUNEL. Compared with the control group, the proliferation of 16HBE cells in CSE group was decreased. Baicalin reversed the effect of 2% CSE on the proliferation of 16HBE cells. Baicalin also reversed the effect of 2% CSE on apoptosis and inflammatory factors in 16HBE cells. miR-125a is highly expressed in COPD, and Baicalin can inhibit the expression of miR-125a. Silencing miR-125a reduces apoptosis and inflammatory response of 16HBE cells in COPD. miR-125a reversed the effects of Baicalin on apoptosis and inflammation of 16HBE cells. Baicalin can reduce CSE-induced apoptosis of human bronchial epithelial cells and release of inflammatory factors, and its mechanism may be related to the inhibition of miR-125a.

Baicalin Weakens the Porcine ExPEC-Induced Inflammatory Response in 3D4/21 Cells by Inhibiting the Expression of NF-κB/MAPK Signaling Pathways and Reducing NLRP3 Inflammasome Activation.

Porcine extraintestinal pathogenic Escherichia coli (ExPEC) is a leading cause of death in pigs and has led to considerable economic losses for the pig industry. Porcine ExPEC infections often cause systemic inflammatory responses in pigs, characterized by meningitis, arthritis, pneumonia, and septicemia. Baicalin has been reported to possess potent anti-inflammatory activity, but its function in porcine ExPEC remains unknown. The aim of this study was to explore the protective effect and mechanism of baicalin against the porcine ExPEC-induced inflammatory responses in 3D4/21 cells. After treatment with baicalin, the effects on cell damage, the level of pro-inflammatory cytokines, the expression of nuclear factor-κB (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathways, and the activation of NOD-like receptor protein 3 (NLRP3) inflammasomes were examined. Our results show that baicalin significantly reduced the damage to 3D4/21 cells infected with porcine ExPEC PCN033. Further study showed that baicalin significantly reduced the transcription and expression of pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-8 (IL-8). Furthermore, baicalin inhibited the phosphorylation of proteins such as P65, nuclear factor κB inhibitor α (IκBα), extracellular regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and P38 and reduced the expression levels of proteins such as NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and caspase-1. These results reveal that baicalin reduced the damage to 3D4/21 cells by inhibiting the expression of NF-κB/MAPK signaling pathways and blocking NLRP3 inflammasome activation in 3D4/21 cells infected with porcine ExPEC. Taken together, these results suggest that baicalin may have potential as a medicine for the treatment of porcine ExPEC-infected pigs by regulating inflammatory responses. This study provides a novel potential pharmaco-therapeutic approach to preventing porcine ExPEC infection.

Regulatory effects of baicalin, a flavonoid compound, on adipocyte metabolism.

Baicalin is a plant-derived, biologically active compound exerting numerous advantageous effects. Adipocytes store and release energy in the process of lipogenesis and lipolysis. Rodent studies have shown that baicalin treatment positively affects fat tissue, however, data on the direct influence of this compound on adipocyte metabolism is lacking. In the present research, the short-term effects of 25, 50, and 100 μM baicalin on glucose transport, conversion to lipids, and oxidation, and also on lipolysis in primary rat adipocytes were explored. Lipolysis was measured as glycerol release from adipocytes. It was shown that 100 μM baicalin reduced glucose oxidation but at any concentration did not affect glucose transport and lipogenesis. Baicalin significantly increased the adipocyte response to physiological and pharmacological lipolytic stimuli (such as epinephrine - adrenergic agonist, DPCPX - adenosine A1 receptor antagonist, and amrinone - cAMP phosphodiesterase inhibitor). The stimulatory effects of baicalin on epinephrine-induced lipolysis were markedly diminished by insulin (activator of cAMP phosphodiesterases) and H-89 (PKA inhibitor). It was also demonstrated that baicalin evoked a similar rise in epinephrine-induced lipolysis in the presence of glucose and alanine. Our results provided evidence that baicalin may reduce glucose oxidation and is capable of enhancing lipolysis in primary rat adipocytes. The action on lipolysis is glucose-independent and covers both the adrenergic and adenosine A1 receptor pathways. The rise in cAMP content is proposed to be responsible for the observed potentiation of the lipolytic process.

Effects of Dietary Supplemental Chlorogenic Acid and Baicalin on the Growth Performance and Immunity of Broilers Challenged with Lipopolysaccharide.

The objective of this study was to investigate the effects of dietary supplemental chlorogenic acid and baicalin (CAB) on the growth performance and immunity of broilers challenged with lipopolysaccharide (LPS). This study was designed as a factorial arrangement of 2 dietary CAB treatments × 2 LPS treatments. Birds challenged with or without LPS were fed with a basic diet (CON) and (LPS), the level of CAB diet containing 500 mg/kg CAB(CAB) and (CAB + LPS). The feeding trial lasted for 42 days. Results showed that there was a negative effect on average daily weight gain (ADG) and average body weight of broilers during the animal trial with LPS challenge. The levels of diamine oxidase (DAO), lysozyme (LYZ), immunoglobulin G (IgG), and IgA in the serum, the contents of IL-1β and TNF-α in the spleen were elevated with LPS treated. Additionally, LPS treatment tended to reduce the jejunal villi height (VH) and total superoxide dismutase (T-SOD) in the serum. Dietary supplemental 500 mg/kg CAB increased the body weight and ADG and improved the feed conversion ratio (FCR) during the trial period. In addition, dietary 500 mg/kg CAB elevated the ratio of VH to crypt depth in the jejunum and reduced the content of protein carbonyl. Beyond that, the levels of IgG and IgA in the serum and transforming growth factor (TGF-β) in the spleen were up-regulated with 500 mg/kg CAB supplementation. In conclusion, dietary CAB was beneficial for growth performance and immunity of broilers challenged with lipopolysaccharide.

Study of the Effect of Baicalin from Scutellaria baicalensis on the Gastrointestinal Tract Normoflora and Helicobacter pylori.

The antimicrobial properties of baicalin against H. pylori and several probiotic cultures were evaluated. Baicalin was isolated from a dry plant extract obtained by extraction with water at 70 °C. For isolation, extraction was carried out with n-butanol and purification on a chromatographic column. The antimicrobial potential was assessed by evaluating changes in the optical density of the bacterial suspension during cultivation; additionally, the disk diffusion method was used. During the study, the baicalin concentrations (0.25, 0.5, and 1 mg/mL) and the pH of the medium in the range of 1.5-8.0 were tested. The test objects were: suspensions of H. pylori, Lactobacillus casei, L. brevis, Bifidobacterium longum, and B. teenis. It was found that the greater the concentration of the substance in the solution, the greater the delay in the growth of the strain zone. Thus, the highest antimicrobial activity against H. pylori was observed at pH 1.5-2.0 and a baicalin concentration of 1.00 mg/mL. In relation to probiotic strains, a stimulating effect of baicalin (1.00 mg/mL) on the growth of L. casei biomass at pH 1.5-2.0 was observed. The results open up the prospects for the use of baicalin and probiotics for the treatment of diseases caused by H. pylori.

Baicalin suppresses colorectal cancer cell proliferation, potentially via ARRDC4: Bioinformatics and experimental analysis

Colorectal cancer (CRC) is a malignant digestive tumor mostly prevalent among adolescents and has great proliferation potential. Baicalin is a flavonoid derived from the dried root of Scutellaria baicalensis, it has tumor-suppressing effects on various kinds of tumors. Although baicalin has been shown to regulate genes associated with CRC, its role in cancer proliferation remains poorly illustrated. In this work, we evaluated the effect of baicalin on the proliferative ability of three CRC cell lines using a cell counting kit-8 assay. Furthermore, we screened for differentially expressed genes in HCT-116 cells using baicalin-treated samples and control samples on a gene expression profile microarray. We identified 19 genes were identified significantly downregulated by baicalin, which may potentially play an indispensable role in the proliferation of HCT-116 cells. High-content screening evaluated whether silencing the 19 genes affected HCT-116 cell growth. The results showed that knocking down ARRDC4 exhibited the most potent inhibition of cell proliferation. ARRDC4 expression was knocked down by transfecting CRC cells with lentiviral shRNA. MTT assay, Caspase-Glo 3/7 assay and immunohistochemistry analysis were performed to explore the effects of baicalin on proliferation and apoptosis of CRC cells. Besides, RT-PCR showed that the expression levels of ARRDC4 mRNA decreased significantly in HCT-116 cells after baicalin treatment. In conclusion, these findings indicated that baicalin may attenuated the expression of ARRDC4 via regulating the levels of LCN2, Claudin-2 and GSTA4 to inhibit HCT-116 cell proliferation. The theoretical underpinnings for the investigation of the pharmacological effects of baicalin in the treatment of human CRC were also established in this study.

Flotation separation of scheelite from calcite using baicalin as a depressant

In this study, the depressive effect and mechanism of baicalin (BAI), a flavonoid, in the flotation separation of scheelite and calcite was investigated. A series of surface analysis techniques were used to explain the selective depression mechanism of BAI on the calcite in flotation. The outcomes of the microflotation tests clearly demonstrated the selective depression of BAI on calcite in flotation separation. Under a pH of 9, dosage regimen of 20 mg/L BAI and 50 mg/L NaOL, the recovery rates were 82.24% for scheelite and 4.12% for calcite. Findings derived from contact angle measurements, adsorption tests, and zeta potential measurements that baicalin impeded the subsequent adsorption of sodium oleate onto calcite after interaction but had a lesser effect on scheelite. Furthermore, analysis of the FTIR spectra and XPS results revealed the selective adsorption of baicalin on the surface of calcite. The dominant component on the calcite surface was mainly positively charged calcium species, the hydroxyl group within the baicalin molecule could chelate react with the calcium plasmonic dots on the calcite surface, it resulting in a stronger chemisorption phenomenon on the calcite surface. But the dominant component on the scheelite surface was mainly negatively charged tungstate, it has less effect on its floatability. Under the inhibiting effect of BAI, the floatability difference between scheelite and calcite becomes larger, and finally achieving the flotation separation of the two minerals. Therefore, BAI is an environmentally friendly and efficient depressant.

Baicalin Antagonizes Prostate Cancer Stemness via Inhibiting Notch1/NF-κB Signaling Pathway.

To investigate the molecular mechanisms underlying the effect of baicalin on prostate cancer (PCa) progression both in vivo and in vitro. The in situ PCa stem cells (PCSCs)-injected xenograft tumor models were established in BALB/c nude mice. Tumor volume and weight were respectively checked after baicalin (100 mg/kg) treatment. Hematoxylin-eosin (HE) staining was used to observe the growth arrest and cell necrosis. mRNA expression levels of acetaldehyde dehydrogenase 1 (ALDH1), CD44, CD133 and Notch1 were determined by reverse transcription-polymerase chain reaction. Protein expression levels of ALDH1, CD44, CD133, Notch1, nuclear factor κB (NF-κB) P65 and NF-κB p-P65 were detected by Western blot. Expression and subcellular location of ALDH1, CD44, CD133, Notch1 and NF-κB p65 were detected by immunofluorescence analysis. In vitro, cell cycle distribution and cell apoptosis of PC3 PCSCs was assessed by flow cytometry after baicalin (125 µmol/L) treatment. The migration and invasion abilities of PCSCs were assessed using Transwell assays. Transmission electron microscopy scanning was utilized to observe the structure and autophagosome formation of baicalin-treated PCSCs. In addition, PCSCs were infected with lentiviruses expressing human Notch1. Compared with the control group, the tumor volume and weight were notably reduced in mice treated with 100 mg/kg baicalin (P<0.05 or P<0.01). Histopathological analysis showed that baicalin treatment significantly inhibited cell proliferation and promoted cell apoptosis. Furthermore, baicalin treatment reduced mRNA and protein expression levels of CD44, CD133, ALDH1, and Notch1 as well as the protein expression of NF-κB p-P65 in the xenograft tumor (P<0.01). In vitro, the cell proliferation of PCSCs was significantly attenuated after treatment with 125 µmol/L baicalin for 72 h (P<0.01). The cell migration and invasion rates were decreased following treatment with baicalin for 48 and 72 h (P<0.01). Baicalin notably induced cell apoptosis and seriously damaged the structure of PCSCs. The mRNA and protein expressions of CD133, CD44, ALDH1 and Notch1 in PCSCs were significantly downregulated following baicalin treatment (P<0.01). Importantly, the inhibitory effects of baicalin on PCa progression and stemness were reversed by Notch1 overexpression (P<0.05 or P<0.01). Mechanistically, baicalin exhibited a potential therapeutic effect on PCa via inhibiting the Notch1/NF-κB signaling pathway and its mediated cancer stemness.

Baicalin promotes random-pattern skin flap survival by inducing autophagy via AMPK-regulated TFEB nuclear transcription.

The random-pattern skin flap is a generally used technique to cover the soft tissue defect, while its application is often constrained by complications after the flap transplant. Necrosis of the flap remains a principal obstacle. The purpose of this study was to investigate the effect of Baicalin on skin flap survival and its mechanism. First of all, we discovered that administering Baicalin stimulated cell migration and boosted the formation of capillary tubes in human umbilical vein endothelial cells. Then, we detected that Baicalin reduced apoptosis-induced oxidative stress by using western blot and oxidative stress test kit. After that, we observed that Baicalin increased autophagy and utilized 3MA to block autophagy augmentation substantially reversing the effects of Baicalin therapy. Furthermore, we uncovered the underlying mechanisms of Baicalin-induced autophagy via AMPK-regulated TFEB nuclear transcription. Finally, our in vivo experiment findings showed that Baicalin reduces oxidative stress, inhibits apoptosis, promotes angiogenesis, and boosts the levels of autophagy. After autophagy was blocked, substantially reversing the effects of Baicalin therapy. Our study indicated that Baicalin-induced autophagy via AMPK regulated TFEB nuclear transcription and then promotes angiogenesis and against oxidative stress and apoptotic promotes skin flap survival. These findings highlight the therapeutic potential for the clinical application of Baicalin in the future.

Protective effect of baicalin against lipopolysaccharideinduced acute lung injury in rats, and the mechanism of action

Purpose: To study the protective influence of baicalin (BA) against LPS-mediated acute lung injury (ALI) in a rat model.&#x0D; Methods: Twenty-seven Sprague-Dawley (SD) rats were assigned (9 rats each) to groups as follows: normal control (NC) treated intraperitoneally with normal saline; lipopolysaccharide (LPS) group treated with 10 mg/kg LPS; and lipopolysaccharide and baicalin (LPS + Ba) group treated with 100 mg/kg LPS, followed 15 min later by 10 mg/kg of baicalin. Pathological changes were assessed by H &amp; E staining. Different types of cells were identified and counted using Rayleigh Giemsa staining. Levels of IL-6 and TNF-α and IL-1β in pulmonary tissue were determined by enzyme-linked immunosorbent assay (ELISA). Matute-Bello scoring method was applied to evaluate the extent of lung injury, while pulmonary expression levels of Nrf2, HO-1 and NQO1 were assayed with Western blot.&#x0D; Results: Lung injury score, and numbers of neutrophils and macrophages were significantly higher in LPS than in NC group. Inflammatory score, and numbers of neutrophils and macrophages in LPS + BA group were significantly lower than those in LPS group (p &lt; 0.05). Compared with NC group, lung tissue levels of IL-6, TNF-α and IL-1β in LPS group were significantly increased, but were significantly reduced in LPS + BA rats, relative to LPS rats (p &lt; 0.05). Expression levels of Nrf2, HO-1 and NQO1 in lung tissue were significantly lower in LPS group than in NC group (p &lt; 0.05) but higher in lung tissue of LPS + BA group, relative to LPS group.&#x0D; Conclusion: Baicalin (BA) protects rats from LPS-induced ALI by enhancing the expressions of Nrf2 and HO-1 through activation of Nrf2/ARE signal pathway. These findings may be useful in developing novel BA-based anti-inflammatory drugs.