Objective To explore the protective effect and mechanism of gardenoside on the damage of dopaminergic neurons induced by lipopolysaccharide (LPS). Methods Both neuron-enriched cultures and neuron-astrocyte cultures were pretreated with vehicle or gardenesides ( 10, 20 and 40 mg/L) for 30 min at 37℃. The culture media were subsequently renewed in order to remove gardenesides. LPS was then added into all culture media at a final concentration of 10 mg/L Twenty-four hours later, the culture media was collected to measure TNF-α, NO, IL-6, GDNF and MMP-9; the cells were collected to count the number of cells labeled with an antibody against tyrosine hydroxylase (TH) and to assess the expression of TH mRNA using reverse transcription-polymerase chain reaction. Results Gardeneside didn't promote the survival of dopaminergic neurons in neuron-enriched culture, but significantly increased the survival of dopaminergic neurons in neuron-astrocyte culture, compared with the vehicle group, the survival of dopaminergic neurons increased from 203.0%±17.4% to 256.7%±15.2% ( F = 17.22, P = 0.001 ) in 40 mg/L gardenaside group. The amount of TNF-α, NO and GDNF released from the neuron-astrocyte cultures after 24 h of addition of LPS was not changed significantly, while the expression of IL-6 and MMP-9 was increased significantly. In this study, the gardenoside concentration-dependently attenuated the LPSinduced increase of the expression of IL-6 and MMP-9, compared with the vehicle group, the expression of IL-6 and MMP-9 decreased to 67.2%±6.4% (F= 12.89,P =0.001 ), 77.3%±9.8% (F =8.27,P = 0.001 ) respectively in 40 mg/L gardenoside group. Conclusions Astrocytes play a neuroprotective role on dopaminergic neurons, which is decreased by LPS via inducing the secretion of pro-inflammatory factors. Gardeneside may protect dopaminergic neurons from LPS-induced injury in an astrocyte-dependent manner and it inhibits the production of proinflammatory factors instead of promoting the secretion of GDNF. From the point of view that a very low toxicity of gardenesides has been well documented, this report may reveal a new way of developing therapeutic interventions for inflammation-related diseases such as Parkinson's disease.

Meridians in human body were classified as white meridian and black meridian according to Tibetan medicine.Season and environment,improper diet,toxic heat and trauma were recognized as main reasons damaging the white meridian in Tibetan Medicine,leading to the emerge of white meridian disease induced by Long (one of the three factors) and blood disorder.White meridian disease in Tibetan medicine involved a series diseases,such as many clinical diseases,due to the damage of white meridian system caused by pathogenic factors.Stroke also belonged to white meridian disease.Drugs and treatments were selected based on the nature of disease such as cold and heat,onset,thelocation of disease and the three factors (Chi Ba,Long and Pei Gen).It was the fundamental principle of the treatment rules of white meridian disease in Tibetan medicine,namely,prescribing medication with the rule of diagnosis and treatment,comprehensive analysis of the causes of diseases and mastering the change law of diseases and syndromes in clinic.

Objective:To investigate the effects of RNA interference(RNAi)-mediated silencing of Peroxiredoxin 1(PRDX1)gene on the invasion and migration of human colorectal cancer SW480 cells.Methods: Lentiviruses negative control vector and PRDX1 RNAi were transfected respectively into colorectal cancer SW480 cells.The transfected cells were divided into PRDX1 silencing group(si-PRDX1)and negative control group(Vector).The expressions of PRDX1 mRNA and protein in SW480 cells were exa mined by quantitative real-time PCR(qRT-PCR)and immunoblotting(Western blot),respectively.The cell migration and invasion capabilities were evaluated with transwell chamber assay and transwell chamber,respectively.The protein expressions of TIMP-2,MMP-2 and MMP-9 were detected by Western blot.Results: Compared with control group,the expressions of PRDX1 mRNA and protein were significantly decreased in PRDX1 silencing group(P<0.01),PRDX1 gene silencing cell line was successfully constructed.The levels of invasion and migration capacities of SW480 cells transfected with si-PRDX1 were lower than those in the cells transfected with control-siRNA(vector)(P<0.01).The expression of TIMP-2 was significantly increased,while the expressions of MMP-2 and MMP-9 were significantly decreased(P<0.05).Conclusion: Silencing of PRDX1 inhibits the invasion,migration and metastasis of human colorectal cancer SW480 cells by regulating the expressions of TIMP-2,MMP-2 and MMP-9.

Objective To investigate the role of astrocyte in the lipopolysaccharide-induced damage of dopaminergic neurons. Methods After lipop01ysaccharide was applied to the third generation of rat astrocytes for 24 hours,supernatants of astrocytes culture were collected.The primary middle-brain dopaminergic neuron-enriched culture systems were obtained by neurobasal and ara-c,eoeulture system of both astrocytes and neurons was established by transwell inserts.The lipopolysaccharide was administered into neuron-enriched systems and coculture systems and the change of dopaminergic neurons was detected.At the same time,the supernatants of astrocytes were administered into the neuron-enriched systems,and the survival of dopaminergic neurons and the expression of tyrosine hydroxylase mRNA were observed. Results Lipopolysaccharide had a negative effect on the survival of dopaminergic neurons in a concentration-dependent manner.Both astrocytes and supernatants promoted the survival of dopaminergie neurons,and the former was better than the latter. In the preoccupation of existence of astrocytes,low-concentration lipopolysaccharide promoted the survival of dopaminergic neurons,while high-concentration,decreased.The change of the expression of tyrosine hydroxylase mRNA was similar to the survival of dopaminergic neurons.Conclusions Astrocytes play a protective role in the damage of dopaminergic neurons induced by lipopolysaccharide,and suitable activation of astrocytes would increase the protective effect while excessive activation of astroeytes would attenuate the effect.

Objective:To evaluate the fetal adrenal gland volume (AGV) and corrected adrenal gland volume (cAGV) in intrauterine growth restriction (IUGR) fetuses and observe their associations with the adverse perinatal outcomes.Methods:From February 2021 to August 2022, 32 IUGR fetuses who underwent fetal ultrasound examination in the Second Xiangya Hospital of Central South University were prospectively selected as the IUGR group, and 32 normal fetuses matched for gestational age during the same period were selected as the control group. Three-dimensional ultrasound was used to obtain fetal adrenal volume images, and the virtual organ computer-aided analysis (VOCAL) was used to measure AGV, then the cAGV was calculated. The values of AGV and cAGV were appropriately compared between the IUGR and the control groups. The pregnancy outcomes were noted. Multiple logistic regression analysis was employed to evaluate the relationship between the cAGV and adverse perinatal outcomes in IUGR fetus, with maternal age and the CPR included as covariates to control for confounding factors.Results:A total of 32 fetuses with IUGR and 32 controls were involved in this prospective study. There was no significant difference in the AGV between these two groups ( P=0.417). The cAGV of the IUGR fetus was substantially larger than that of the normal fetus ( P=0.034). In the multivariate logistic regression analysis, after adjusting for maternal age and fetal CPR, the fetal cAGV was noticeably associated with the fetal distress (adjusted OR=0.005, 95% CI=0.000-0.587, P=0.029) and the total adverse perinatal outcomes (adjusted OR=0.014, 95% CI=0.000-0.475, P=0.018). Conclusions:The value of cAGV is increased in the IUGR fetuses and associated with adverse perinatal outcomes. The evaluation of fetal AGV could be beneficial to monitoring and managing IUGR fetuses.

Objective:To explore the effect of probiotics on the cognitive function of patients with schizophrenia.Methods:100 schizophrenic patients admitted to Shanghai Jinshan District Mental Health Center from January 2019 to January 2021 were randomly divided into the conventional group (treated with atypical antipsychotics combined with placebo, 50 cases) and the intervention group (treated with atypical antipsychotics combined with probiotics, 50 cases). Before treatment and 3 months after treatment, the feces of the patients were taken for DNA detection to compare the composition of intestinal flora. The cognitive function of the patients was assessed by the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), and the mental state of the patients was assessed by the Positive and Negative Symptom Scale(PANSS). The incidence of adverse drug reactions was compared between the two groups.Results:Before treatment, the relative abundance of Fusobacteria, Proteus and Actinobacteria in the two groups had no statistical significant difference (all P>0.05); After 3 months of treatment, the relative abundance of Fusobacteria, Proteus and Actinobacteria in the two groups decreased compared with that before treatment, and the decline was more significant in the intervention group (all P<0.05). Before treatment, there was no significant difference in immediate memory, visual span, speech function, attention function, delayed memory and RBANS between the two groups (all P>0.05); After 3 months of treatment, the scores of immediate memory, visual span, speech function, attention function, delayed memory and RBANS in the two groups were higher than those before treatment, and the increase was more significant in the intervention group (all P<0.05). Before treatment, there was no significant difference in PANSS scores between the two groups ( P>0.05); After 3 months of treatment, PANSS scores in both groups decreased compared with those before treatment, and the decrease degree in the intervention group was higher than that in the conventional group (all P<0.05). During the three months of treatment, there was no significant difference in the incidence of adverse drug reactions between the two groups ( P>0.05). Conclusions:Probiotics are used in adjuvant therapy for patients with schizophrenia, which can regulate the patients′ intestinal flora, improve patients′ cognitive function and mental disorders, and do not increase the incidence of adverse drug reactions. They have significant clinical efficacy and high treatment safety.

Objective To investigate the clinical diagnostic value of plasma serine protease inhibitor Ka-zal-type 4(SPINK4)expression in colorectal adenocarcinoma(CRC)and progressive adenoma(AA).Methods A total of 62 patients with CRC(CRC group)and 15 patients with AA(AA group)diagnosed by colonoscopy and pathological examination in this hospital from June 2020 to December 2021 were selected,and 22 healthy people undergoing physical examination during the same period were selected as the HC group.The expression of SPINK4 in plasma was detected by ELISA,and the expression of CEA in plasma was detected by electrochemiluminescence,and the correlation was analyzed.The diagnostic efficiency was analyzed by re-ceiver operating characteristic(ROC)curve,and the expression of p53 in CRC tissues was detected by immu-nohistochemistry.Results The expression of plasma SPINK4 in the CRC group and AA group was lower than that in the HC group(Z=3.72,-0.41,P＜0.05),and the expression of CEA in the CRC group was higher than that in the HC group(Z=-3.63,P＜0.05).The area under the curve(AUC),accuracy,sensi-tivity and specificity of SPINK4 combined with CEA in the diagnosis of CRC and AA were higher than those of SPINK4 and CEA alone.The positive rate of mutant type p53 in SPINK4 low expression group and CEA high ex-pression group was significantly increased in CRC patients(72.55％,75.00％,P＜0.05).Conclusion The expression of plasma SPINK4 is decreased in CRC and AA,and the combined detection of SPINK4 and CEA has a good di-agnostic efficiency in CRC and AA.