Advances in traditional Chinese medicine for respiratory disease therapy in 2021

Respiratory diseases are common conditions that endanger human health.Their etiology,pathogenesis,and prognosis are complex,and clinical research has been extensive.This paper reviews studies from the PubMed database to assess the progress of traditional Chinese medicine in the treatment of respiratory diseases in 2021,focusing on related animal and cell models of coronavirus disease 2019.Traditional Chinese medicine extracts,such as polysaccharides and emodin,and classic prescriptions,such as Mahuang decoction,respond to the treatment of influenza by reducing viral infections and regulating the body’s immune response.Chinese herbal extracts,such as schizandra B and andrographolide,treat asthma by inhibiting inflammatory response pathway formation,NLRP3 inflammasome formation,oxidative stress,and autophagy.Traditional Chinese medicine extracts such as fucoxanthin,and proprietary Chinese medicines such as the Xihuang pill is used in the treatment of lung cancer,as it regulates the cell cycle,inhibit tumor cell proliferation,and enhance the body’s immune function.Classic formulas such as the kidney tonic lung formula and proprietary Chinese medicine,such as compound grass stone silkworm granules,relieve airway inflammation and improve lung function in chronic obstructive pulmonary disease.Chinese herbal extracts,such as jostilbene and sage phenol,inhibit epithelial cell-mesenchymal transformation and regulate the levels of inflammatory factors to treat idiopathic pulmonary fibrosis to provide a reliable basis for the treatment of respiratory diseases.

Therapeutic effect of secretome from TNF-αstimulated mesenchymal stem cells in an experimental model of corneal limbal stem cell deficiency

AIM:To explore the secretome efficacy in tumor necrosis factor(TNF)-αstimulated mouse mesenchymal stem cells(MSCs)in a murine model of corneal limbal alkali injury.METHODS:Corneal limbal stem cell deficiency(LSCD)was created in the eyes of male C57 mice.Concentrated conditioned medium from TNF-αstimulated MSCs(MSC-CMT)was applied topically for 4 wk,with basal medium and conditioned medium from MSCs as controls.Corneal opacification,corneal inflammatory response,and corneal neovascularization(NV)were evaluated.Corneal epithelial cell apoptosis,corneal conjunctivation,and inflammatory cell infiltration were assessed with TUNEL staining,CK3 and Muc-5 AC immunostaining,and CD11 b immunofluorescence staining,respectively.The effect of TSG-6 was further evaluated by knockdown with short hairpin RNA(sh RNA).RESULTS:Compared to the controls,topical administration of MSC-CMT significantly ameliorated the clinical symptoms of alkali-induced LSCD,with restrained corneal NV,reduced corneal epithelial cell apoptosis,and inhibition of corneal conjunctivation.In addition,MSC-CMT treatment significantly reduced CD11 b+inflammatory cell infiltration,and inhibited the expression of pro-inflammatory cytokines(IL-1β,TNF-αand IL-6).Furthermore,the promotion of corneal epithelial reconstruction by MSC-CMT was largely abolished by TSG-6 knockdown.CONCLUSION:Our study provides evidence that MSCCMT enhances the alleviation of corneal alkali injuries,partially through TSG-6-mediated anti-inflammatory protective mechanisms.MSC-CMT may serve as a potential strategy for treating corneal disorders.

Mufangji tang ameliorates pulmonary arterial hypertension through improving vascular remodeling,inhibiting inflammatory response and oxidative stress,and inducing apoptosis

Background:Mufangji tang(MFJT)is composed of Ramulus Cinnamomi,Radix Ginseng,Cocculus orbiculatus(Linn.)DC.,and Gypsum.In clinical settings,MFJT has been effectively employed in addressing a range of respiratory disorders,notably including pulmonary arterial hypertension(PAH).However,the mechanism of action of MFJT on PAH remains unknown.Methods:In this study,a monocrotaline-induced PAH rat model was established and treated with MFJT.The therapeutic effects of MFJT on PAH rat model were evaluated.Network pharmacology was conducted to screen the possible targets for MFJT on PAH,and the molecular docking between the main active components and the core targets was carried out.The key targets identified from network pharmacology were tested.Results:Results showed significant therapeutic effects of MFJT on PAH rat model.Analysis of network pharmacology revealed several potential targets related to apoptosis,inflammation,oxidative stress,and vascular remodeling.Molecular docking showed that the key components were well docked with the core targets.Further experimental validation results that MFJT treatment induced apoptosis(downregulated Bcl-2 levels and upregulated Bax levels in lung tissue),inhibited inflammatory response and oxdative stress(decreased the levels of IL-1β,TNF-α,inducible NOS,and malondialdehyde,and increased the levels of endothelial nitric oxide synthase,nitric oxide,glutathione and superoxide dismutase),reduced the proliferation of pulmonary arterial smooth muscle cells(downregulated ET-1 andβ-catenin levels and ERK1/2 phosphorylation,increased GSK3βlevels).Conclusion:Our study revealed MFJT treatment could alleviate PAH in rats via induction of apoptosis,inhibition of inflammation and oxidative stress,and the prevention of vascular remodeling.

Ala-Gln improves varicocele-induced testicular injury by increasing HSP70 and antioxidant activity in male rats

This worked aimed to test the hypothesis that L-alanyl-L-glutamine(Ala-Gln)improves the varicocele-induced testicular injury,which causes male infertility.For this purpose,fifty adult male Wistar rats received the varicocele(VC)surgery at the left renal vein.Biomarkers were determined 2,4,and 8 weeks after VC(n=10/each detection).Four weeks after VC,rats received Ala-Gln(1.125 g/kg)treatment with and or saline for 1 week(n=10/each group).Rats in the sham group were also detected for biomarkers at 2,4,and 8 weeks(n=10/each detection).VC caused testicular injury detected by hematoxylin–eosin(H&E)staining,immunohistochemistry,and TUNEL assay.HSP70 mRNA was detected quantitative RT-PCR,SOD,and CAT by nitroblue tetrazolium(NBT)method and 8-OHDG by ELISA.The results showed that varicocele induced injury in the testes.The weight of the left testes was lower than that of the right testes in VC-bearing rats(p<0.01).The relative numbers of sustentacular and spermatogenic cells were decreased after VC(p<0.01).In sham-4 wk,VC-4wk,VC-5wk and Ala-Gln groups,the apoptosis index was 5.10±1.14,13.22±3.63,33.62±3.56 and 22.33±2.61,relative level of HSP70 mRNA 1.00±0.12,0.53±0.05,0.51±0.04 and 1.62±0.15 fold,SOD 16.4±0.23,13.4±0.17,10.01±1.06 and 19.53±2.26 U/mg protein,CAT 2.16±0.31,1.07±0.28,and 1.31±0.26 and 3.46±0.71 U/mg,8-OHDG 5.23±0.67,6.81±0.78,7.16±1.22 and 4.14±0.73 pg/μg DNA,respectively(p<0.01).Our results suggest that Ala-Gln prevented the VC-induced testicular injury.We have firstly reported that Ala-Gln protects against varicocele-induced testicular injuries by up-regulation of HSP70 and antioxidants,SOD and CAT,and down-regulation of oxidant 8-OHDG,resulting in reducing apoptosis in the testis.

TGF-β2-induced NEAT1 regulates lens epithelial cell proliferation,migration and EMT by the miR-26a-5p/FANCE axis

AIM:To explore the regulatory mechanism of nuclear paraspeckle assembly transcript 1(NEAT1)in the pathogenesis of posterior capsule opacification(PCO).METHODS:Quantitative reverse transcription polymerase chain reaction(RT-q PCR)was executed to analyze NEAT1 and micro RNA(miR)-26a-5p expression in transforming growth factor-beta 2(TGF-β2)-disposed lens epithelial cells(LECs).The proliferation,cell cycle progression,apoptosis,and migration of TGF-β2-disposed LECs were evaluated.The relationship between NEAT1 or fanconi anemia(FA)complementation group E(FANCE)and miR-26a-5p was verified by dual-luciferase reporter assay.RESULTS:TGF-β2 induced NEAT1 expression in LECs.NEAT1 inhibition accelerated apoptosis,cell cycle arrest,decreased proliferation,epithelial-mesenchymal transition(EMT),and migration of TGF-β2-disposed LECs.NEAT1 sponged miR-26a-5p to further regulate FANCE expression.Rescue experiments presented that miR-26a-5p downregulation overturned NEAT1 silencing-mediated impacts on TGF-β2-disposed LEC biological behaviors.Additionally,FANCE overexpression reversed miR-26a-5p mimic-mediated impacts on TGF-β2-disposed LEC biological behaviors.CONCLUSION:TGF-β2-induced NEAT1 facilitates LEC proliferation,migration,and EMT by upregulating FANCE via sequestering miR-26a-5p.

A hippocampal anti-hypertensive mechanism induced by twirling reinforcing-reducing manipulation in rats

Objective:To investigate a hippocampal anti-hypertensive mechanism induced by twirling reinforcingreducing manipulation(TRRM)using proteomics in rats.Methods:Forty-two male spontaneously hypertensive rats were randomly divided into 3 groups,and 14 Wistar-Kyoto rats were served as control group.In the twirling reinforcing(TRF)group,needles were directly inserted into the Taichong(LR 3)point,then thumbs were moved heavily forward and lightly backward for 3 min,while needles remained inserted for 17 min.In the twirling reduction(TRD)group,the same treatment was applied as in the TRF group except that the thumb moved lightly forward and heavily backward.In the model and control groups,only the corresponding grasping and fixation were applied.All interventions were conducted for 14 days.The blood pressure(BP)of all rats was measured one day before intervention and every other day after.Then hematoxylin-eosin(H&E)staining,label-free and parallel reaction monitoring proteomic techniques were used to assess hippocampal samples from each group.Results:Systolic BPs showed a significant decrease in the TRF and TRD groups compared with the model group(P<.01).In the model group,H&E staining showed obvious pathological changes in the hippocampus,while in the TRF and TRD groups,the hippocampal morphology was only slightly altered.Labelfree proteomic analysis revealed 1163 differential protein expressions between groups.Gene Ontology enrichment analysis confirmed that the differentially expressed proteins were enriched in different biological processes,cellular components,and molecular functions.Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that TRRM proteins were expressed in the serotonergic synapse pathway,renin-angiotensin system,the mitogen-activated protein kinase signaling pathway,and the peroxisome pathway,which were all also related to BP regulation.Conclusion:TRRM can significantly lower the BP of SHRs.The mode of action may be through the activation of various protein pathways in the hippocampus that are related to BP regulation.

Gastric signet-ring cell carcinoma with paraneoplastic eosinophilia: A case report and literature review

We report the case of a 40-year-old female Chinese patient with gastric signet-ring cell carcinoma that was first diagnosed because of paraneoplastic eosinophilia.The patient’s eosinophil count reduced markedly to normal levels within 24 h after radical gastrectomy and Billroth II anastomosis.The patient recovered well after the surgery and no abnormalities were found during the regular follow-ups.Paraneoplastic eosinophilia is an unusual manifestation that usually remains asymptomatic;moreover,cases of solid malignant tumors with eosinophilia are uncommon.To our knowledge,this is the first reported case of paraneoplastic eosinophilia in a patient with gastric carcinoma.We considered eosinophilia as a manifestation of a paraneoplastic syndrome,which can be the first clinical manifestation of a malignancy.

Polycystic ovary syndrome and intestinal flora

Polycystic ovary syndrome(PCOS)is a condition in which a woman has increased levels of male hormones(androgens).Many problems occur as a result of this increase of hormones,including:Menstrual irregularitiesInfertility,Skin problems such as acne and increased hair growth,Increased number of small cysts in the ovaries.