Depression is a prevalent mental and emotional disor-der that often results in significant emotional disturbances,cog-nitive dysfunction,and memory impairments.It is characterized by a high incidence rate,a substantial disability burden,and limited therapeutic efficacy.Currently,the long-term use of medications for the treatment of depression can result in a range of adverse reactions,highlighting the urgent need to explore no-vel approaches that can effectively alleviate depressive symptoms while minimizing side effects.Curcumin,a natural polyphenolic compound derived from the rhizome of turmeric,demonstrates considerable potential in the prevention and treatment of depres-sion,owing to its diverse array of biological activities.In recent years,numerous studies have investigated the use of curcumin for the treatment of depression.This article aims to provide a comprehensive review of the mechanisms of action underlying curcumin's efficacy in treating depression.Specifically,it focu-ses on its ability to improve neurotransmitter imbalances,restore neural plasticity,alleviate neural damage,mitigate dysfunction of the hypothalamic-pituitary-adrenal(HPA)axis,regulate in-flammatory factors and neuroinflammatory signaling pathways,and inhibit oxidative stress.This review is intended to offer in-sights and methodological references for basic research on curcu-min,as well as for the development of novel therapeutic agents for the treatment of depression.

Objective To investigate the effect and mechanism of long non-coding RNA(lncRNA)NRON on myocardial fibrosis in mice with myocardial infarction(MI).Methods Thirty-two C57/BL6 mice were randomly assigned to a Sham group,MI group,MI+shNRON group or MI+NC group,with eight mice in each group.The expression level of lncRNA NRON in myocardial tissue of mice was detected by real-time quantitative PCR.Hematoxylin and eosin staining,Masson's trichrome staining,and immunohistochemistry were used to detect the degree of myocardial injury,myocardial fibrosis,and the expression level of collagen Type Ⅰ(col Ⅰ).Western blotting was used to detect the protein expression levels of TGF-β1,p-Smad2,and p-Smad3 in myocardial tissue of the mice.Results Compared with the Sham group,the expression of NRON,col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were increased in the MI group.Compared with the MI group,the expression of NRON,the degree of myocardial damage and fibrosis,the expression of col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were decreased in the MI+shNRON group.Conclusion Down-regulation of lncRNA NRON can alleviate myocardial injury and inhibit myocardial fibrosis in mice with MI,and the molecular mechanism may be related to inhibition of the TGF-β/Smad signaling pathway.

The application of botulinum neurotoxin(BoNT)in cosmetic procedures of the head and neck is well established.In recent years,however,its therapeutic scope has significantly expanded to include functional and pathological disorders within this anatomical region.This article reviews the use of BoNT as an important treatment modality for various head and neck disorders,encompassing movement disor-ders(such as laryngeal,craniocervical,middle ear,oromandibular,and cervical dystonia),peripheral nerve dysfunction(including multiple system atrophy,migraine,synkinesis and spasm following facial nerve palsy),upper aerodigestive tract dysfunction(e.g.,post-laryngectomy complications,cricopharyn-geal dysphagia,pharyngeal pouch,and retrograde cricopharyngeal dysfunction),and autonomic nervous disorders(such as sialorrhea and gustatory sweating syndrome).By leveraging its highly specific neuro-modulatory effects,BoNT provides a reversible,minimally invasive,and potent therapeutic alternative for conditions often refractory to conventional pharmacological or surgical interventions.This review systemat-ically examines the mechanisms of action,injection techniques,clinical efficacy,and safety profiles of BoNT in the above-mentioned diseases,and discusses future applications,aiming to offer comprehensive evidence-based guidance for clinical practice to otolaryngologists-head and neck surgeons.

Objective To investigate the effect and mechanism of long non-coding RNA(lncRNA)NRON on myocardial fibrosis in mice with myocardial infarction(MI).Methods Thirty-two C57/BL6 mice were randomly assigned to a Sham group,MI group,MI+shNRON group or MI+NC group,with eight mice in each group.The expression level of lncRNA NRON in myocardial tissue of mice was detected by real-time quantitative PCR.Hematoxylin and eosin staining,Masson's trichrome staining,and immunohistochemistry were used to detect the degree of myocardial injury,myocardial fibrosis,and the expression level of collagen Type Ⅰ(col Ⅰ).Western blotting was used to detect the protein expression levels of TGF-β1,p-Smad2,and p-Smad3 in myocardial tissue of the mice.Results Compared with the Sham group,the expression of NRON,col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were increased in the MI group.Compared with the MI group,the expression of NRON,the degree of myocardial damage and fibrosis,the expression of col Ⅰ,TGF-β1,p-Smad2,and p-Smad3 proteins were decreased in the MI+shNRON group.Conclusion Down-regulation of lncRNA NRON can alleviate myocardial injury and inhibit myocardial fibrosis in mice with MI,and the molecular mechanism may be related to inhibition of the TGF-β/Smad signaling pathway.

The application of botulinum neurotoxin(BoNT)in cosmetic procedures of the head and neck is well established.In recent years,however,its therapeutic scope has significantly expanded to include functional and pathological disorders within this anatomical region.This article reviews the use of BoNT as an important treatment modality for various head and neck disorders,encompassing movement disor-ders(such as laryngeal,craniocervical,middle ear,oromandibular,and cervical dystonia),peripheral nerve dysfunction(including multiple system atrophy,migraine,synkinesis and spasm following facial nerve palsy),upper aerodigestive tract dysfunction(e.g.,post-laryngectomy complications,cricopharyn-geal dysphagia,pharyngeal pouch,and retrograde cricopharyngeal dysfunction),and autonomic nervous disorders(such as sialorrhea and gustatory sweating syndrome).By leveraging its highly specific neuro-modulatory effects,BoNT provides a reversible,minimally invasive,and potent therapeutic alternative for conditions often refractory to conventional pharmacological or surgical interventions.This review systemat-ically examines the mechanisms of action,injection techniques,clinical efficacy,and safety profiles of BoNT in the above-mentioned diseases,and discusses future applications,aiming to offer comprehensive evidence-based guidance for clinical practice to otolaryngologists-head and neck surgeons.

Streptococcus equinus is a zoonotic disease that can cause illness in various animals under specific environmental condi-tions.No reports have described isolation of this bacterium from the liver in affected sheep.This study successfully isolated and identi-fied a strain of Streptococcus equinus through bacterial isolation and culture,Gram staining,drug sensitivity testing,mouse sensitivity testing,bacterial biochemical testing,and whole genome sequencing.The strain was found to have pathogenicity toward Kunming white mice,and to be sensitive to four antibiotics(penicillin,ampicillin,ceftiofur sodium,and ceftriaxone sodium)but resistant to four antibiotics(streptomycin,amoxicillin,tetracycline,and gentamicin).On the basis of drug sensitivity testing,targeted treatment of the affected sheep flock with ceftiofur sodium effectively controlled the disease within 2 days,and no new cases occurred.This study provides a reference for biological characterization of ovine Streptococcus equinus;public health;and the investigation of disease pre-vention,control,and epidemiology.

Objective To investigate the effect of Nde1 gene knockout on early neural development of zebrafish by visualizing the development of neural networks in zebrafish.Methods Transgenic zebrafish Tg(Nde1-/-;HuC:RFP+/-)was constructed by crossing Nde1-/-with Tg(HuC:RFP+/-).The HuC promoter was employed to drive the expression of red fluorescent protein in neurons,which allowing the visualization of zebrafish neural networks and tracking of neural development.Furthermore,by using Image J and Prism to compare the average fluorescence intensity of neurons and the expression level of fluorescent reporter proteins between Nde1 deficiency zebrafish and wild type zebrafish,the effect of Nde1 gene knockout on zebrafish neural development was analyzed.Results From 48 hours post-fertilization(hpf)to 7 days dpf,the average fluorescence intensity of red fluorescence expressed by trigeminal sensory neurons and spinal cord neurons in Nde1 deficiency zebrafish was lower than that in wild type zebrafish.RT-qPCR results also showed that the mRNA expression level of red fluorescent reporter protein in Nde1 deficiency zebrafish was significantly lower than that in the wild type zebrafish.Conclusion Nde1 gene deletion may lead to abnormal development of trigeminal sensory neurons and spinal cordneurons by affecting neural progenitor cell differentiation and increasing apoptosis.

This study investigated the effects of Rehmanniae Radix Praeparata on striatal neuronal apoptosis in rats with attention deficit hyperactivity disorder(ADHD) based on the B-cell lymphoma-2(Bcl-2)/Bcl-2-associated X protein(Bax)/caspase-3 signaling pathway. Twenty-four 3-week-old male spontaneously hypertensive rats(SHR) were randomly divided into a model group, a methylphenidate group(2 mg·kg~(-1)·d~(-1)), and a Rehmanniae Radix Praeparata group(2.4 mg·kg~(-1)·d~(-1)). Age-matched male Wistar Kyoto(WKY) rats were used as the normal control group, with 8 rats in each group. The rats were administered by gavage for 28 days. Body weight and food intake were recorded for each group. The open field test and elevated plus maze test were used to assess hyperactivity and impulsive behaviors. Nissl staining was used to detect changes in striatal neurons and Nissl bodies. Terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL) fluorescence staining was used to detect striatal cell apoptosis. Western blot was employed to detect the expression levels of Bcl-2, Bax, and caspase-3 proteins in the striatum. The results showed that compared with the model group, Rehmanniae Radix Praeparata significantly reduced the total movement distance, average movement speed, and central area residence time in the open field test, and significantly reduced the ratio of open arm entries, open arm stay time, and head dipping in the elevated plus maze test. Furthermore, it increased the number of Nissl bodies in striatal neurons, significantly downregulated the apoptosis index, significantly increased Bcl-2 protein expression and the Bcl-2/Bax ratio, and reduced Bax and caspase-3 protein expression. In conclusion, Rehmanniae Radix Praeparata can reduce hyperactivity and impulsive behaviors in ADHD rats. Its mechanism may be related to the regulation of the Bcl-2/Bax/caspase-3 signaling pathway in the striatum, enhancing the anti-apoptotic capacity of striatal neurons.
Animals ; Male ; Apoptosis/drug effects* ; Rats ; Drugs, Chinese Herbal/administration & dosage* ; Caspase 3/genetics* ; Proto-Oncogene Proteins c-bcl-2/genetics* ; bcl-2-Associated X Protein/genetics* ; Rehmannia/chemistry* ; Attention Deficit Disorder with Hyperactivity/physiopathology* ; Signal Transduction/drug effects* ; Neurons/cytology* ; Rats, Inbred SHR ; Rats, Inbred WKY ; Humans ; Corpus Striatum/cytology* ; Plant Extracts