Probiotic cocktails accelerate baicalin metabolism in the ileum to modulate intestinal health in broiler chickens

Background Baicalin and probiotic cocktails are promising feed additives with broad application prospects.While probiotic cocktails are known to enhance intestinal health,the potential synergistic impact of combining baicalin with probiotic cocktails on the gut health of broiler chickens remains largely unexplored.Therefore,this study aims to investigate the influence of the combined administration of baicalin and probiotic cocktails on the composition of ileal and cecal microbiota in broiler chickens to elucidate the underlying mechanisms responsible for the healthpromoting effects.Results A total of 3201-day-old male Arbor Acres broilers were divided into 4 groups,each with 8 replicates of 10 chicks per replicate.Over a period of 42 d,the birds were fed a basal diet or the same diet supplemented with 37.5 g/t baicalin(BC),1,000 g/t probiotic cocktails(PC),or a combination of both BC(37.5 g/t)and PC(1,000 g/t).The results demonstrated that BC+PC exhibited positive synergistic effects,enhancing intestinal morphology,immune function,and barrier function.This was evidenced by increased VH/CD ratio,sIgA levels,and upregulated expression of occludin and claudin-1(P<0.05).16S rRNA analysis indicated that PC potentiated the effects of BC,particularly in the ileum,where BC+PC significantly increased theα-diversity of the ileal microbiota,altered itsβ-diversity,and increased the relative abundance of Flavonifractor(P<0.05),a flavonoid-metabolizing bacterium.Furthermore,Flavonifractor positively correlated with chicken ileum crypt depth(P<0.05).While BC+PC had a limited effect on cecal microbiota structure,the PC group had a very similar microbial composition to BC+PC,suggesting that the effect of PC at the distal end of the gut overshadowed those of BC.Conclusions We demonstrated the synergistic enhancement of gut health regulation in broiler chickens by combining baicalin and probiotic cocktails.Probiotic cocktails enhanced the effects of baicalin and accelerated its metabolism in the ileum,thereby influencing the ileal microbiota structure.This study elucidates the interaction mechanism between probiotic cocktails and plant extract additives within the host microbiota.These findings provide compelling evidence for the future development of feed additive combinations.

Attenuation of the Activation of NLRP3 Inflammasome in Fibroblast Like Synoviocytes of Rheumatoid Arthritis by Baicalin through Regulating the Let-7i-3p/PI3K/Akt/NF-κB Signaling Axis

[Objectives]To study the effect and mechanism of baicalin on the activation of NLRP3 inflammasome in human fibroblast like synoviocytes of rheumatoid arthritis(HFLS-RA).[Methods]To confirm that baicalin alleviated the activation of NLRP3 inflammasome in HFLS-RA,the expression of NLRP3 before and after baicalin treatment was observed by immunofluorescence.Western blot was used to detect the protein expression of p-PI3K,p-Akt,NF-κB p65,NLRP3,ASC and caspase-1 after baicalin treatment for 48 h,and the contents of IL-1 and IL-18 in the supernatents were detected by ELISA.In order to explore the mechanism of baicalin alleviating the activation of NLRP3 inflammasome,the corresponding relationship between let-7i-3p and PIK3CA was verified by double luciferin and Westen blot analysis.The expression of let-7i-3p and PI3K before and after baicalin intervention was detected by RT-qPCR.let-7i-3p interference was used to verify whether baicalin mitigated the activation of enhanced NLRP3 inflammasome.[Results]Baicalin(50 and 100 mg/L)significantly reduced the activation of NLRP3 inflammasome,inhibited the protein expressions of p-PI3K,p-Akt,NF-κB p65,NLRP3,ASC and caspase-1,and the secretion of IL-1 and IL-18.let-7i-3p and PIK3CA had a targeted correspondence,and baicalin up-regulated the expression of let-7i-3p and down-regulated the expression of PIK3CA.Baicalin attenuated the activation of NLRP3 inflammasome enhanced by let-7i-3p interference.[Conclusions]Baicalin can up-regulate let-7i-3p expression,inhibit PI3K/Akt/NF-κB signal transduction,and thus reduce the activation of NLRP3 inflammasome in HFLS-RA.

Effect of Baicalin on TNBS-Induced Colonic Inflammatory Injury in Rats

Objective: The aim is to observe the protective effect of baicalin on trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis in mice and explore its mechanism. Methods: The mice were divided into 4 groups: ethanol control group, TNBS model group, baicalin low-dose group and baicalin high-dose group. The model of experimental colitis in mice was induced by TNBS enema. After 2 hours of TNBS enema, baicalin was given by gavage, QD × 7D. The animals were sacrificed on the 8th day to observe the extent of colonic mucosal damage, and the Peroxidase activity, Malondialdehyde (MDA) and glutathione (GSH) contents were measured. Results: Compared with the TNBS model group, the body weight, gross injury score and histological changes were significantly improved;MPO enzyme activity and MDA content were significantly decreased in the low and high-dose baicalin groups;and the content of glutathione increased. Conclusion: Baicalin can alleviate TNBS-induced colitis in mice, and the mechanism is related to the antioxidation of baicalin.

Baicalin:a prominent therapeutic agent against colorectal cancer

The occurrence and development of colorectal cancer involve multiple genes and pathways as a result of accumulated mutations at several sites that control growth and differentiation.Baicalin is a flavonoid extracted from Scutellaria baicalensis Georgi with antioxidant,anti-inflammatory and antiviral activities.Here,we discuss its possible clinical development and perspectives for future research.We also summarize the literature on colorectal cancer as well as the anticancer effect of Scutellaria baicalensis Georgi in the last 20 years.As research progresses,the therapeutic effect of baicalin in combating colorectal cancer has gradually been recognized.Its impact on colorectal cancer and anticancer mechanism,such as blocking the tumor cell cycle,inducing tumor cell apoptosis,preventing and treating tumor metastasis and anti-inflammatory activity,have become new hot topics in the study of antitumor agents in Chinese medicine.The present review surveys and summarizes studies of baicalin in anti-colorectal cancer treatment to enhance the understanding of its tumoricidal mechanism and to provide new therapeutic options for colorectal cancer.

Anti-bacterial mechanism of baicalin-tobramycin combination on carbapenem-resistant Pseudomonas aeruginosa

BACKGROUND Pseudomonas aeruginosa(P.aeruginosa)is an important cause of nosocomial infections,and contributes to high morbidity and mortality,especially in intensive care units.P.aeruginosa is considered a'critical'category bacterial pathogen by the World Health Organization to encourage an urgent need for research and development of new antibiotics against its infections.AIM To investigate the effectiveness of baicalin combined with tobramycin therapy as a potential treatment method for carbapenem-resistant P.aeruginosa(CRPA)infections.METHODS Polymerase chain reaction(PCR)and RT-PCR were used to detect the expression levels of drug-resistant genes(including VIM,IMP and OprD2)and biofilmrelated genes(including algD,pslA and lasR)in CRPA that confer resistance to tobramycin,baicalin and tobramycin combined with baicalin(0,1/8,1/4,1/2 and 1MIC).RESULTS There was a correlation between biofilm formation and the expression of biofilmrelated genes.In addition,VIM,IMP,OprD2,algD,pslA and lasR that confer biofilm production under different concentrations in CRPA were significantly correlated.The synergistic effect of baicalin combined with tobramycin was a significant down-regulation of VIM,IMP,algD,pslA and lasR.CONCLUSION Baicalin combined with tobramycin therapy can be an effective treatment method for patients with CRPA infection.

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

BACKGROUND 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.AIM To investigate the potential role of autophagy in LiCl-pilocarpine-induced SE.METHODS 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.Furthermore,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).RESULTS 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.CONCLUSION We illustrated that Baicalin-induced activation of autophagy alleviates apoptotic death and protects the hippocampus of SE rats.

Effects of baicalin in CD4 + CD29 + T cell subsets of ulcerative colitis patients

AIM:To evaluate the role of baicalin in ulcerative colitis(UC) with regard to the CD4+CD29+ T helper cell,its surface markers and serum inflammatory cytokines.METHODS:Flow cytometry was used to detect the percentage of CD4+CD29+ cells in patients with UC.Real time polymerase chain reaction was used to detect expression of GATA-3,forkhead box P3,T-box expressed in T cells(T-bet),and retinoic acid-related orphan nuclear hormone receptor C(RORC).Western blotting was used to analyze expression of nuclear factor-κB(NF-κB) p65,phosphorylation of NF-κB(p-NF-κB) p65,STAT4,p-STAT4,STAT6 and p-STAT6.The concentrations of interferon-γ(IFN-γ),interleukin(IL)-4,IL-5,IL-6,IL-10 and TGF-β in serum were determined by ELISA assay.RESULTS:The percentages of CD4+CD29+ T cells were lower in treatment with 40 and 20 μmol/L baicalin than in the treatment of no baicalin.Treatment with 40 or 20 μmol/L baicalin significantly upregulated expression of IL-4,TGF-β1 and IL-10,increased p-STAT6/STAT6 ratio,but downregulated expression of IFN-γ,IL-5,IL-6,RORC,Foxp3 and T-bet,and decreased ratios of T-bet/GATA-3,p-STAT4/STAT4 and p-NF-κB/NF-κB compared to the treatment of no baicalin.CONCLUSION:The results indicate that baicalin regulates immune balance and relieves the ulcerative colitis-induced inflammation reaction by promoting proliferation of CD4+CD29+ cells and modulating immunosuppressive pathways.

Nerve protective effect of Baicalin on newborn HIBD rats

Objetive:To investigate the nerve protective effect and mechanism of baicalin on newborn rats with hypoxic ischemic brain damage(HIBD).Methods:A total of 64 SD newborn rats were randomlu divided into control group.model group.nerve growth factor group and baicalin group.with 16 in each group.Left carotid artery ligation method was adopted to establish the HIBD model except fou in control group,which was treatde with intraperitoneal injection of salin e10mL/kg for 3 d.After oxygen recovery on hypoxia ischemia rats.intraperitoneal injectionof salin 10mL/kg was adopted in model group for 3 d.Intraperitoneal injection of nerve growth factor injection50μg/kg per day was adopted in nerve growth factor group for 3 d:intraperitoneal injection of radix scutellariae 16mg/kg per day was adopted in baicalin group for 3 d after modeeling.Four rats of each group were sacrificed at Day 1,2,3,7 for microscopic observation of pathological morphological changes in brain tissus aften HE staining,S-P immunohistochemical method was used for observation of Fas and FasL expression in brain cells.Results:Neat structure of cells was observed in control group;edema cells in disordered arrangement was observed in model group,with some cells necrosis and cavity change;tissue injury in nerve growth factor group and baicalin group was significantly lighter than that in model group;Fas and FasL expression in model group,nerve growth factor group and baicalin group were significantiy higher than that in control group at different time points(P<0.05):Fas and FasL expression in nerve growth factor group and baicalin group were significantly lower than that in model group at different time points(P<0.05):There was no statistical diggerence of Fas,FasL expression at each time point between nerve growth factor group and baicalin group(P>0.05).Conclusions:Baicalin can reduce expression of Fas and FasL in HIBD rats,inhibit apoptosis of nerve cells,thus achieve the protective effect on HIBD rat nerves.

Baicalin attenuates blood-spinal cord barrier disruption and apoptosis through PI3K/Akt signaling pathway after spinal cord injury

Baicalin is a natural active ingredient isolated from Scutellariae Radix that can cross the blood-brain barrier and exhibits neuroprotective effects on multiple central nervous system diseases.However,the mechanism behind the neuroprotective effects remains unclear.In this study,rat models of spinal cord injury were established using a modified Allen's impact method and then treated with intraperitoneal injection of Baicalin.The results revealed that Baicalin greatly increased the Basso,Beattie,Bresnahan Locomotor Rating Scale score,reduced blood-spinal cord barrier permeability,decreased the expression of Bax,Caspase-3,and nuclear factorκB,increased the expression of Bcl-2,and reduced neuronal apoptosis and pathological spinal cord injury.SH-SY5 Y cell models of excitotoxicity were established by application of 10 m M glutamate for 12 hours and then treated with 40μM Baicalin for 48 hours to investigate the mechanism of action of Baicalin.The results showed that Baicalin reversed tight junction protein expression tendencies(occludin and ZO-1)and apoptosis-related protein expression(Bax,Bcl-2,Caspase-3,and nuclear factor-κB),and also led to up-regulation of PI3 K and Akt phosphorylation.These effects on Bax,Bcl-2,and Caspase-3 were blocked by pretreatment with the PI3 K inhibitor LY294002.These findings suggest that Baicalin can inhibit bloodspinal cord barrier permeability after spinal cord injury and reduce neuronal apoptosis,possibly by activating the PI3 K/Akt signaling pathway.This study was approved by Animal Ethics Committee of Xi'an Jiaotong University on March 6,2014.

Baicalin and deferoxamine alleviate iron accumulation in different brain regions of Parkinson's disease rats

Previous studies found that iron accumulates in the substantia nigra of Parkinson＇s disease patients However, it is still unclear whether other brain regions have iron accumulation as well. In this experiment, rats with rotenone-induced Parkinson＇s disease were treated by gastric perfusion of baicalin or intraperitoneal injection of deferoxamine. Immunohistochemical staining demonstrated that iron accumulated not only in the substantia nigra pars compacta, but also significantly in the striatum globus pallidus, the dentate gyrus granular layer of the hippocampus, the dentate-interpositus and the facial nucleus of the cerebellum. Both baicalin and deferoxamine, which are iron chelating agents, significantly inhibited iron deposition in these brain areas, and substantially reduced the loss of tyrosine hydroxylase-positive cells. These chelators also reduced iron content in the substantia nigra. In addition to the substantia nigra, iron deposition was observed in other brain regions as well. Both baicalin and deferoxamine significantly inhibited iron accumulation in different brain regions, and had a protective effect on dopaminergic neurons.

Baicalin influences the dendritic morphology of newborn neurons in the hippocampus of chronically stressed rats

Chronic stress models, established in adult Sprague-Dawley rats through a 14-day subcutaneous injection of 40 mg/kg corticosterone, once per day, were given a daily oral feeding of 50 mg/kg baicalin. The study was an attempt to observe the effect of baicalin on neurogenesis in chronically stressed rats. Results showed that subcutaneous injection of corticosterone significantly decreased the total number of doublecortin-positive neurons in the hippocampus. The reduced cell number caused by corticosterone was mainly due to the decrease of class II doublecortin-positive neurons, but the class I doublecortin-positive neurons were unaffected. Baicalin treatment increased the number of both class I and class II doublecortin-positive neurons. In addition, doublecortin-positive neurons showed less complexity in dendritic morphology after corticosterone injection, and this change was totally reversed by baicalin treatment. These findings suggest that baicalin exhibits a beneficial effect on adult neurogenesis.

Baicalin interferes with iron accumulation in C6 glioma cells

Baicalin reacts with ferric ammonium citrate and acts as an-iron chelator. The maximal reaction time for baicalin to interact with irons was approximately 3 hours. C6 glioma cell survival decreased following iron-loading, with a large number of cells accumulating iron. In addition, lipid peroxidation increased. Iron accumulation and lipid peroxidation were the major cause of cellular death. Baicalin and ferric ammonium citrate alleviated iron accumulation in C6 cells and lowered the mortality of nerve cells. In addition, malondialdehyde and lactate dehydrogenase levels reduced. These results indicate that baicalin strongly inhibits lipid peroxidation via chelation, reduces the content of iron in C6 cells, lowers lipid peroxidation, and thus plays a protective role against iron-induced nerve cell death.

Baicalin inhibits colistin sulfate-induced apoptosis of PC12 cells

Baicalin, a type of flavonoid extracted from the dried root of Scutellaria baicalensis georgi, has been shown to effectively inhibit cell apoptosis. Therefore, we assumed that baicalin would suppress colistin sulfate-induced neuronal apoptosis. PC12 cells exposed to colistin sulfate （62.5-500 μg/mL） for 24 hours resulted in PCl2 cell apoptosis. In addition, caspase-3 activity, lactate dehydrogenase level and free radical content increased in a dose-dependent manner. Subsequently, PC12 cells were pretreated with baicalin （25, 50 and 100 pg/mL）, and exposed to 125 pg/mL colistin sulfate. Cell morphology markedly changed, and cell viability increased. Moreover, caspase-3 activity, lac- tate dehydrogenase level and free radical content decreased. Results indicated that baicalin inhib- ited colistin sulfate-induced PC12 cell apoptosis by suppressing free radical injury, and reducing caspase-3 activity and lactate dehydrogenase activity.

Pathological changes in multiple organs of rats with severe acute pancreatitis treated by baicalin and octreotide

BACKGROUND: Severe acute pancreatitis (SAP) features fatal pathogenetic conditions and high mortality rate. The study of SAP complicated with multiple organ injuries is of important significance. In this study, we explored the protective effect of baicalin on multiple organs of SAP rats and compared it with that of octreotide through light and electron microscopic observations of the pathological changes. METHODS: The improved Aho method was used to prepare SAP rat models. These rats were then randomly divided into a sham-operated group (n=45), a model control group (n=45), baicalin-treated group (n=45) and octreotide-treated group (n=45). Based on the difference in time points after operation, these groups were subdivided into 3, 6 and 12 hour subgroups (n=15). At the corresponding time point after operation, the mortality rate of rats was recorded, and then the rats were humanely killed to take samples of multiple organs that were subsequently examined for pathological changes under light and electron microscopy. RESULTS: At 12 hours after operation, the mortality rate of rats in the baicalin- and octreotide-treated groups was lower than that in the model control group (P < 0.05). Compared to the model control group, the pathological changes and pathological scores in the baicalin- and octreotide-treated groups were mitigated and relieved to varying degrees. The pathological changes under electron microscopy were also improved. CONCLUSIONS: Both baicalin and octreotide show good protective effects on multiple organs of SAP rats. Baicalin as a new drug has good prospects in the treatment of SAP.

Pharmacokinetic Characteristics of Baicalin in Rats with 17α-ethynylestradiol-induced Intrahepatic Cholestasis

Baicalin is one of the main active ingredients of choleretic traditional Chinese medicine drug Radix Scutellariae.The aim of this study was to explore the pharmacokinetic characteristics of baicalin in rats with 17α-ethynylestradiol（EE）-induced intrahepatic cholestasis（IC） based on its choleretic effects.Firstly,rats were subcutaneously injected with EE solution（5 mg/kg,0.25 m L/100 g） for 5 consecutive days to construct an IC model.Then the bile excretion rate,serum levels of alanine aminotransferase（ALT）,aspartate aminotransferase（AST）,alkaline phosphatase（ALP） and total bile acid（TBA） and pathological changes of the liver were detected.Secondly,after successfully modeling,the rats were intragastrically given baicalin solution（200 mg/kg）（n=6）.Blood samples were collected from the tail vein at different time points after intragastric administration.The protective effects of low-（50 mg/kg）,medium-（100 mg/kg） and high-dose（200 mg/kg） baicalin on the liver in IC rats were evaluated.The content of baicalin in plasma was detected by liquid chromatography-mass spectrometry/mass spectrometry and pharmacokinetics parameters were calculated.Pharmacodynamic results showed that low-,medium-and high-dose baicalin all significantly increased the average excretion rate of bile（P〈0.05）,and significantly decreased serum levels of ALT,AST and ALP and TBA（P〈0.05）.Meanwhile,HE staining showed that baicalin significantly relieved EEinduced hepatocyte edema and necrosis.Pharmacokinetic results exhibited that the absorption of baicalin in both IC and normal control rats showed bimodal phenomenon.Cmax,AUC（0-t） and AUC（0-∞） of baicalin in IC rats were significantly higher than those of the normal control group（P〈0.01）.T1/2 of plasma baicalin in the model group was significantly extended to（11.09±1.84） h,with clearance dropping to 61.78% of that of the normal control group（P〈0.01）.The above results suggested that baicalin had protective effects on the liver of IC rats,accompanied by significantly increased in vivo exposure,delayed in vivo clearance and markedly alterative pharmacokinetic characteristics.This study provides a theoretical basis for further development of baicalin as a feasible drug for treating IC.Key words

Baicalin suppresses iron accumulation after substantia nigra injury: relationship between iron concentration and transferrin expression

Previous studies have shown that baicalin prevented iron accumulation after substantia nigra injury, reduced divalent metal transporter 1 expression, and increased ferroportin 1 expression in the substantia nigra of rotenone-induced Parkinson＇s disease rats. In the current study, we investigated the relationship between iron accumulation and transferrin expression in C6 cells, to explore the mechanisms of the inhibitory effect of baicalin on iron accumulation observed in Parkinson＇s disease rats. Iron content was detected using inductively coupled plasma-atomic emission spectroscopy. Results showed that iron content decreased 41% after blocking divalent metal transporter 1 and ferroportin 1 proteins. After treatment with ferric ammonium citrate of differing concentrations （10, 50, 100, 400 ktg/mL） in C6 glioma cells, cell survival rate and ferroportin 1 expression were negatively correlated with ferric ammonium citrate concentration, but divalent metal transporter 1 expression positively correlated with ferric ammonium citrate concentration. Baicalin or deferoxamine reduced divalent metal transporter 1 expression, but increased ferroportin 1 expression in the 100 μg/mL ferric ammonium citrate-loaded C6 cells. These results indicate that baicalin down-regulated iron concentration, which positively regulat- ed divalent metal transporter 1 expression and negatively regulated ferroportin 1 expression, and decreased iron accumulation in the substantia nigra.

Role of baicalin as a potential therapeutic agent in hepatobiliary and gastrointestinal disorders:A review

Baicalin is a natural bioactive compound derived from Scutellaria baicalensis,which is extensively used in traditional Chinese medicine.A literature survey demonstrated the broad spectrum of health benefits of baicalin such as antioxidant,anticancer,anti-inflammatory,antimicrobial,cardio-protective,hepatoprotective,renal protective,and neuroprotective properties.Baicalin is hydrolyzed to its metabolite baicalein by the action of gut microbiota,which is further reconverted to baicalin via phase 2 metabolism in the liver.Many studies have suggested that baicalin exhibits therapeutic potential against several types of hepatic disorders including hepatic fibrosis,xenobiotic-induced liver injury,fatty liver disease,viral hepatitis,cholestasis,ulcerative colitis,hepatocellular and colorectal cancer.During in vitro and in vivo examinations,it has been observed that baicalin showed a protective role against liver and gut-associated abnormalities by modifying several signaling pathways such as nuclear factor-kappa B,transforming growth factor beta 1/SMAD3,sirtuin 1,p38/mitogen-activated protein kinase/Janus kinase,and calcium/calmodulin-dependent protein kinase kinaseβ/adenosine monophosphate-activated protein kinase/acetyl-coenzyme A carboxylase pathways.Furthermore,baicalin also regulates the expression of fibrotic genes such as smooth muscle actin,connective tissue growth factor,β-catenin,and inflammatory cytokines such as interferon gamma,interleukin-6(IL-6),tumor necrosis factor-alpha,and IL-1β,and attenuates the production of apoptotic proteins such as caspase-3,caspase-9 and B-cell lymphoma 2.However,due to its low solubility and poor bioavailability,widespread therapeutic applications of baicalin still remain a challenge.This review summarized the hepatic and gastrointestinal protective attributes of baicalin with an emphasis on the molecular mechanisms that regulate the interaction of baicalin with the gut microbiota.

Baicalin modulates microRNA expression in UVB irradiated mouse skin

This study aimed to evaluate the effects of baicalin on ultraviolet radiation B （UVB）-mediated microRNA （miRNA） expression in mouse skin. We determined miRNA expression profiles in UVB irradiated mice, baicalin treated irradiated mice, and untreated mice, and conducted TargetScan and Gene Ontology analyses to predict miRNA targets. Three miRNAs （mmu-miR-125a-5p, mmu-miR-146a, and mmu-miR-141） were downregulated and another three （mmu-miR-188-5p, mmu-miR-223 and mmu-miR-22） were upregulated in UVB irradiated mice compared with untreated mice. Additionally, these miRNAs were predicted to be related to photocarcinogenesis, hypomethylation and apoptosis. Three miRNAs （mmu-miR-378, mmu-miR-199a-3p and mmu-miR-181b） were downregulated and one （mmu-miR-23a） was upregulated in baicalin treated mice compared with UVB irradiated mice, and they were predicted to be related to DNA repair signaling pathway. These deregulated miRNAs are potentially involved in the pathogenesis of photodamage, and may aid treatment and prevention of UVB-induced dermatoses.

Protective effects of baicalin on amyloid beta 25-35-induced apoptosis in human neuroblastoma SH-SY5Y cells

Baicalin, a type of flavanoid, effectively prevents cellular apoptosis induced by various factors. However, little evidence is available regarding its role on amyloid β （Aβ） -induced neuronal apoptosis. The present study investigated the protective mechanisms of baicalin on Aβ-induced neuronal apoptosis. Flow cytometry and cation dye 5, 5＇, 6, 6＇-tetrachloro-1, 1＇, 3, 3＇-tetraethyl- benzimidazoly lcarbocyanine iodide （JC-1） were employed to measure mitochondrial membrane potential, and nitric oxide secretion and apoptotic-related factors, such as caspase-3, were comprehensively analyzed. Results demonstrated a protective effect of baicalin on Aβ-treated SH-SY5Y cell viability; the rate of apoptosis decreased, nitric oxide generation and expression of caspase-3 were effectively inhibited, and mitochondrial membrane potential was effectively protected. Baicalin inhibited Aβ-induced neuronal apoptosis via multiple targets and multiple pathways, such as the inhibition of free radical damage, reduction of caspase-3 expression, and protection of normal mitochondrial functions.

Baicalin treatment regulates hyperactivity of HPA axis and alters SIRT1 related inflammation in the hypothalamus in a model of depression

OBJECTIVE Hyperactivityof hypothalamic-pituitary-adrenal(HPA) axis is an important aetiological risk factor for the development of depression. Previous studies have demonstrated that the phenolic monomer baicalin has antidepressant-like effects and decreases serum corticosterone levels.However,the mechanism by which baicalin regulates hyperactivity of HPA axis remains unclear. This work aimed to investigate the effects of baicalin on hyperactivity of HPA axis using the olfactory bulbectomised(OBX) rat model of depression. METHODS Animals were anaesthetised with 10% chloral hydrate(3.3 mL·kg^(-1),ip). Using disinfected surgical equipment,the skull covering the olfactory bulbs was exposed by a midline incision. Two burr holes(2 mm diameter) were drilled 8 mm anterior to the bregma and 2 mm lateral to the midline. Both olfactory bulbs were aspirated and the holes filled with glass ionomer cement. The scalp was sutured closed. Sham-operated rats underwent every surgical procedure except the aspiration of the bulbs. The animals received penicillin(8×10~5U) intramuscularly(0.2 mL/300 g) once per day for 3 d post-surgery to prevent infection,and were subsequently housed alone in polypropylene cages. The experiments continued after 14 d of rehabilitation. The following groups were used for experiments: sham-operated(underwent surgical procedure without aspiratedolfactory bulbs and administration of vehicle only),OBX-model(underwent every surgical procedure and administration of vehicle only),OBX-amitriptyline treated(10 mg·kg^(-1)),and OBX-baicalin treatment(20 and 40 mg·kg^(-1)). Amitriptyline and baicalin were dissolved in physiological saline. RESULTS We examined how baicalin altered OBX-induced changes in serum glucocorticoid level as wel as inflammatory responses,sirtuin 1(SIRT1) expression,and p65 acetylation in the hypothalamus. Similar experiments were performed to analyse the effects of baicalin on lipopolysaccharide-induced inflammatory responses inhypothalamus. CONCLUSION Our results indicate that activation of the SIRT1 in the hypothalamus contributes to hyperactivity of HPA axis,which can be alleviated by baicalin.