Animals ; Astrocytes ; metabolism ; Brain Ischemia ; metabolism ; pathology ; Glial Fibrillary Acidic Protein ; metabolism ; Neuroprotective Agents ; pharmacology ; Propofol ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; prevention & control

Animals ; Disease Models, Animal ; Electric Stimulation ; Neurons ; metabolism ; Nitric Oxide Synthase ; metabolism ; Parkinson Disease ; metabolism ; Rats ; Subthalamic Nucleus ; metabolism

OBJECTIVETo observe the effect of Jianpi Bushen Qingchang Huashi Recipe (JBQHR) on proliferation and migration of bone marrow mesenchymal stem cells (BMSCs).

METHODSBMSCs were isolated and cultured in vitro with adherence screening method to prepare cell suspension. No drug intervention was given to BMSCs in the vehicle control group. JBQHR at 0.39, 0.78, 1.56 µg/mL was added in BMSCs of low, mid, and high dose JBQHR groups for co-incubation. Its effect on the proliferation of BMSCs was detected by CCK-8. BMSCs migration and chemotactic ability was detected using Transwell method. Each dose JBQHR combined ERK kinase inhibitor U0126 was set up as control. The phosphorylation of extracellular regulated protein kinase (ERK) and CAMP responsive element-binding protein (CREB) were detected by Western blot.

RESULTSCompared with the vehicle control group, the proliferation of BMSCs and BMSCs migration number could be promoted in the 3 JBQHR groups (P < 0.05). Besides, the proliferation of BMSCs was better in mid and high dose JBQHR groups than in the low dose JBQHR group (P < 0.05). Compared with the vehicle control group, the phosphorylation of ERK and CREB could be elevated in the 3 JBQHR groups (P < 0.05), and could be inhibited by U0126 (P < 0.01). Compared with the low dose JBQHR group, the phosphorylation of ERK increased in mid and high dose JBQHR groups with statistical difference (P < 0.05).

CONCLUSIONJBQHR could promote the proliferation and migration of BMSCs, and its mechanism might be related to ERK/CREB signaling pathway

Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Humans ; MAP Kinase Signaling System ; Mesenchymal Stromal Cells ; cytology ; drug effects

AIMTo observe the change of STR neuronal firing rates with high frequency stimulation of subthalamic nucleus in PD rats.

METHODSA model of Parkinson's disease was induced by unilateral administration of 6-hydroxydopamine into right substantia nigra in rats. After the high-frequency stimulation to STN, the spontaneous firing rates of STR on normal and PD rats were recorded by using extracellular recordings.

RESULTSStimulation caused a direct excited effect of STR neurons in normal rats whereas a excited and inhibited effect in PD rats. The inhibited effect was correlated with the stimulation period (r = 0.94).

CONCLUSIONStimulation to STN may inhibit the spontaneous firing rates of STR neurons in PD rats. These results also give some clues that high-frequency stimulation to STN may be a effective therapy to the clinical treatment of Parkinson's disease.

Action Potentials ; Animals ; Corpus Striatum ; physiopathology ; Disease Models, Animal ; Electric Stimulation Therapy ; Male ; Neurons ; physiology ; Parkinson Disease ; physiopathology ; therapy ; Rats ; Rats, Sprague-Dawley ; Subthalamic Nucleus

Animals ; Dentate Gyrus ; metabolism ; Epilepsy ; chemically induced ; metabolism ; Glial Fibrillary Acidic Protein ; metabolism ; Hippocampus ; metabolism ; Kainic Acid ; Male ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins ; metabolism ; Neurons ; metabolism ; Neuropeptides ; metabolism

OBJECTIVETo investigate the effect of penehyclidine hydrochloride on glutamate (Glu)release and N-methyl-D-aspartate receptor (NMDAR)1 expression in hippocampus CA1 with global cerebral ischemia/reperfusion rats.

METHODSSixty male Wistar rats were randomly allocated into three groups; group A received sham operation; group B received ischemia/reperfusion; group C received penehyclidine hydrochloride treatment (2 mg/kg) before ischemia/reperfusion (n=20). Global cerebral ischemia was induced according to Pulsinelli-Brierley method. All animals were divided into two experiments: (I) Microdialysis plus HPLC/FD were used to detect Glu level after reperfusion 1 h, 3 h, 6 h. (II) After reperfusion 3 h, the animals were decapitated on ice and the brains were immediately removed to detect NMDAR1 expression in CA1 area by immunohistochemistry.

RESULTSAfter penehyclidine hydrochloride treatment, extracellular Glu level in CA1 were significantly decreased compared with those of control group (P < 0.05 or 0.01); Total integrated OD, average gray value and positive-cell area of NMDAR1 in CA1 were also significantly decreased compared with those of control group (P < 0.05 or 0.01).

CONCLUSIONPenehyclidine hydrochloride might has protective effect in hippocampus CA1 on global cerebral ischemia/reperfusion animals. The protective mechanism might be involved in inhibiting Glu release and NMDAR1 expression.

Animals ; Brain Ischemia ; metabolism ; physiopathology ; CA1 Region, Hippocampal ; metabolism ; Cholinergic Antagonists ; pharmacology ; Glutamic Acid ; metabolism ; Male ; Quinuclidines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; metabolism ; Reperfusion Injury ; metabolism ; prevention & control

Silver-Russell syndrome ( SRS ) is a rare genetic disorder with non-specific manifestations and severity , so that the clinical diagnosis of SRS remains difficult.We reported a 23-year-old female patient with SRS characterized with short body stature , asymmetry, obesity, fifth finger clinodactyly and dislocation of hip .The patient had a past history of lengthening operation on the right lower limb at the age of 10.Chromosome analysis revealed (46, XX).The patient was admitted due to severe asymmetry in low extremities caused by right-side obesity .After successful orthopedic surgery in the right hips and thighs the symptoms of patient were relieved .

Sepsis is a potentially fatal condition characterized by the failure of one or more organs due to a disordered host response to infection. The development of sepsis is closely linked to immune dysfunction. As a result, immunotherapy has gained traction as a promising approach to sepsis treatment, as it holds the potential to reverse immunosuppression and restore immune balance, thereby improving the prognosis of septic patients. However, due to the highly heterogeneous nature of sepsis, it is crucial to carefully select the appropriate patient population for immunotherapy. This review summarizes the current and evolved treatments for sepsis-induced immunosuppression to enhance clinicians' understanding and practical application of immunotherapy in the management of sepsis.

Objective To study the influences of mental disorders on female systemic lupus erythematosus(SLE)and analyze the factors. Methods We used symptom check list -90 (SCL-90) as a basis for judging mental disorders disease activity. Disease activity, social support and depreciation - discrimination were used as possible influencing factors. Social support and discomfort – discrimination were possible influencing factors. Multivariate unconditional logistic regression model was used to analyze the influencing factors of mental disorders. Results The total score of SCL-90 of patients with female SLE was significantly higher than that of norm models ［(136.39±48.66) vs (129.96±38.76)］ (P<0.05), in 289 SLE patients, the number of patients with mental disorders was 128 (44.3%). High monthly income(OR=0.770, 95% CI:0.604-0.981, P=0.034) was a protective factor for mental disorders. High disease activity (OR=1.792, 95% CI:1.023-3.138, P=0.042)and high discomfort–discrimination (OR=1.100, 95% CI:1.035-1.169, P=0.002)were risk factors for mental disorders. Conclusions Female SLE patients have a higher risk of mental disorders than the general population. And eliminating self-depreciation, reducing social discrimination, active employment, increasing monthly income, standardizing treatment and reducing disease activity may effectively alleviate mental disorders in SLE patients.

BACKGROUND: Role of Wnt/β-catenin signaling pathway in the pathogenesis of osteoarthritis has been proved by numerous animal experiments and human specimen trials. Wnt/β-catenin signaling pathway and matrix metalloproteinase 13 (MMP-13) play important roles in pathological process of osteoarthritis, and they may be related with each other. OBJECTIVE: To detect the expression levels of β-catenin and MMP-13 in the synovial tissue of osteoarthritis, and to investigate the relationship between β-catenin and MMP-1 in the pathogenesis of osteoarthritis. METHODS: Synovial tissues were obtained from the 54 patients undergoing total knee arthroplasty or knee arthroscopic diagnosis and treatment surgery and 12 healthy patients suffering from amputation caused by trauma. The samples were divided into non-, mild-, medium-and severe-osteoarthritis groups based on advanced Mankin scores. The expression levels of β-catenin and MMP-13 in the synovial tissues were detected by immunohistochemistry, and correlation analysis was conducted. RESULTS AND CONCLUSION: Immunohistochemistry results showed that MMP-13 was negative in the non-osteoarthritis group, positive in 5 (50%) samples in the mild-osteoarthritis group, positive in 11 (65%) samples in the medium-osteoarthritis group and positive in 23 (85%) samples in the severe-osteoarthritis group. β-Catenin was positive in 1 (8%) sample in the non-osteoarthritis group, positive in 7 (70%) samples in the mild-osteoarthritis group, positive in 14 (82%) samples in the medium-osteoarthritis group and positive in 25 (93%) samples in the severe-osteoarthritis group. The expression levels of β-catenin and MMP-13 in the synovial tissues presented a positive correlation (r=0.806, P ＜ 0.001), and the levels increased with joint degeneration becoming severe. These results imply that there is a significant increase in the expression levels of β-catenin and MMP-13 in the synovial tissues of osteoarthritis compared with the non-osteoarthritis group, and β-catenin and MMP-13 exert effects in development of osteoarthritis. Beta-catenin and MMP-13 are closely associated with pathological changes such as cartilage degeneration and synovial inflammation, thus providing new theoretical direction and experimental basis for targeted gene therapy of osteoarthritis.