Connerlevin5147

05).

Icariin increased the bone mass and improved the condition of the defect area in the rabbit skulls.

Icariin increased the bone mass and improved the condition of the defect area in the rabbit skulls.

To investigate the protective effects of electroacupuncture and LGNHFD on cerebral ischemia-reperfusion injury, and their effects on the expression of cluster of differentiation 34 (CD 34), vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) in the peripheral tissue of the cerebral ischemic semi-dark zone in rats. The influence and mechanism of expression.

Healthy male Sprague-Dawley rats were randomly divided into the sham operation group, model group, Traditional Chinese Medicine (TCM) group, electroacupuncture group, and acupuncture group. The cerebral ischemia model was prepared by middle artery occlusion. The electroacupuncture and TCM groups received electroacupuncture at the ""Neiguan (PC6)"", ""Baihui (GV20)"", and ""Renzhong (GV26)"" acupoints from 4 h after modeling, once daily for 14 d. After modeling, the acupuncture and TCM groups were administered LGNHFD once daily for 14 d. After treatment, the infarct volume and regional cerebral blood flow (rCBF) were measation - in the ischemic hemispheres of such rats.

Acupuncture therapy is superior to simple drug and electroacupuncture therapy for reducing infarct volume, increasing rCBF and CD34 expression in cells, and promoting capillary regeneration in rats with cerebral ischemia. This may be related to the increased expression of VEGF, bFGF, and CD34 - which are related to cerebrovascular neovascularization - in the ischemic hemispheres of such rats.

To investigate the protective efficacy of electroacupuncture (EA) pretreatment at Neiguan (PC6) on myocardial ischemia-reperfusion (I/R) in rats.

Fifty rats were randomly divided into five groups (n = 10) sham operation group, model group (underwent in vivo myocardial I/R), EA pretreatment group [EA at Neiguan (PC 6) 1 week before I/R], wortmannin group (1 week before I/R, the PI3K inhibitor, wortmannin, was injected), EA pretreatment + wortmannin group (both pretreatments were performed simultaneously). ROCK inhibitor After establishing the I/R model, 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to analyze the weight and area of the myocardial infarction tissue. The biosignal and pressure test system was used to determine the left ventricular systolic mean pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), fractional shortening (FS), and ejection fraction (EF). Ultraviolet spectrophotometry was used to determine the expression of creatine kinase (CK)-MB, inducible nitric oxide synthase (iNreatment slightly widened the myocardial fiber space, reduced necrosis and myocardial cell swelling and maintained the nucleus and mitochondria structure intact.

EA pretreatment promoted autophagy flux and alleviated myocardial I/R injury through the PI3K-Akt-mTOR pathway.

EA pretreatment promoted autophagy flux and alleviated myocardial I/R injury through the PI3K-Akt-mTOR pathway.

To investigate the efficacy of Zhuifeng tougu capsules (, ZFTG) in the treatment of rheumatoid arthritis (RA) in rats and study its mechanism, focusing on the toll-like receptor 2/4-nuclear factor kappa-B (TLR2/4-NF-κB) signaling pathway.

Type Ⅱ collagen and an artificial climate box were used to construct the rat model of collagen-induced arthritis with wind-cold-dampness arthralgia syndrome. The rats were divided randomly into a control group, wind-cold-dampness syndrome model group, and high-, medium-, and low-dose ZFTG groups. The methotrexate (MTX) control group was treated with the corresponding drug intervention for 28 d. The joint temperature, pain threshold, joint swelling degree, and arthritis index (AI) score were measured. The production of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and rheumatoid factors (RFs) in the blood was detected by enzyme-linked immunosorbent assay. The protein expression of TLR2, TLR4, and NF-κB in synovial tissues was detected by Western blotting, and the mRNA expression of TLR2, TLR4, and NF-κB was detected by real-time polymerase chain reaction.

Compared with the model group, the joint temperature in each treatment group, the MTX control group, and MTX group recovered, the degree of foot swelling, pain threshold, AI score decreased, serum CRP, ESR, RF level and the levels of TLR2, TLR4, and NF-κB in synovial tissue were decreased (P < 0.05). Among them, the curative effect in the medium-dose and MTX groups was more evident (P < 0.01).

ZFTG has a significant effect on RA in rats, and its mechanism may involve regulating CRP levels, the ESR, and RFs via the TLR2/4-NF-κB signaling pathway.

ZFTG has a significant effect on RA in rats, and its mechanism may involve regulating CRP levels, the ESR, and RFs via the TLR2/4-NF-κB signaling pathway.

To observe the behavioral changes and changes in DNA fragments and related inflammatory factors in the hippocampus of epileptic rats pretreated with Rongchang capsule ().

Eighty Sprague-Dawley rats were randomly divided into the normal group (NG), model group (MG), sodium valproate group (VG), and Rongchang capsule group (RG) (n = 20 in each group). Pentylentetrazol was administered to the MG, VG, and RG to induce epilepsy. The VG and RG were pretreated with 1/2 the therapeutic dose of sodium valproate and Rongchang capsule, respectively. Changes in convulsion behavior and water maze learning were observed. Single cell gel electrophoresis was used to detect changes in the DNA in the hippocampus. The tail length (TL) and Olive tail moment (OTM) of cells were analyzed by GASP software. The expression of interleukin-1β (IL-1β), high mobility group box 1 (HMGB1), transforming growth factor-β (TGF-β), and CCL4 in the hippocampus was determined by Western blotting.

Rongchang capsule had a weaker effect on conule prevents or delays cognitive impairment in rats with induced epilepsy, reduces hippocampal DNA damage, and decreases the hippocampal expressions of IL-1β, CCL4, and HMGB1.

Pretreatment with Rongchang capsule prevents or delays cognitive impairment in rats with induced epilepsy, reduces hippocampal DNA damage, and decreases the hippocampal expressions of IL-1β, CCL4, and HMGB1.