Efficacy of herb-partitioned moxibustion at Qihai(CV 6) and bilateral Tianshu(ST 25) on colonic damage and the TLR4/NF-κB signaling pathway in rats with Crohn's disease

OBJECTIVE: To observe the effect of stimulating Qihai(CV 6) and bilateral Tianshu(ST 25) with herb-partitioned moxibustion(HPM) in rats with Crohn's disease(CD), and to investigate the possible anti-inflammatory mechanism of HPM.METHODS: Forty rats were randomly divided into four groups(n = 10 rats per group): normal control(NC), model control(MC), mesalamine(MES), and HPM. The CD rat model was established in the MC,MES, and HPM groups by administering a mixture of trinitrobenzenesulfonic acid and alcohol via enema. The HPM group received HPM on Qihai(CV 6)and bilateral Tianshu(ST 25), while the MES group received intragastric mesalamine. Colonic histomorphological scores, and serum concentrations of tumor necrosis factor α(TNF-α) and interleukin 1β(IL-1β) were assessed to evaluate the effects of HPM on colonic reparation and anti-inflammation.The expressions of Toll-like receptor 4(TLR-4), nuclear factor κB inhibitor α(IκB-α), IκB kinase α/β(IKKα/β), and NF-κB p65 were further analyzed to investigate the regulatory effects of the interventions on the TLR4/NF-κB pathway.RESULTS: CD rats showed inflammatory colonic damage and increased serum concentrations of TNF-α and IL-1β. The expressions of TLR4, IKKα/β,and NF-κB p65 in the colons of CD rats were significantly increased compared with the NC group,while the expression of IκBα(a key negative regulator of NF-κB p65) was decreased. HPM significantly mitigated colonic damage and reduced the serum concentrations of TNF-α and IL-1β. HPM downregulated the expressions of TLR4, IKKα/β, and NF-κB p65 in the colon, and upregulated the expression of IκBα. The effects of HPM in CD rats were similar to those of mesalamine.CONCLUSION: HPM alleviates colonic inflammation in CD rats. This may be achieved through regulation of TLR4, which induces NF-κB signal transduction.     

慢性ITP外周血单个核细胞Th1/Th2亚群反应状态及生血灵干预研究

目的探讨辅助性T淋巴细胞亚群Th1、Th2在慢性特发性血小板减少性紫癜(ITP)发病中的作用,观察生血灵对慢性ITP Th1、Th2亚群功能状态的影响。方法以酶联免疫吸附法(ELISA法)检测慢性ITP患者外周血单个核细胞(PBMC)培养上清中Th1型细胞因子IL-2和Th2型细胞因子IL-10的水平。结果慢性ITP患者PBMC培养上清中IL-2和IL-10的含量均较正常对照组明显减低(P均<0.001),生血灵对其具有明显提升作用(P<0.01)。结论慢性ITP患者Th亚群免疫功能低下。生血灵治疗慢性ITP能够增强Th亚群免疫功能,恢复其平衡。     

普洱茶籽的化学成分研究

普洱茶籽乙醇提出物的正丁醇萃取部分,经酸水解后,分离出5种成分,经光谱和化学分析,分别鉴定为二十八烷烃,柚皮素和3种新酯酰基皂甙元22-O-当归酸酯茶皂甙元B,22-O-当归酸酯茶皂甙元E和22-O-当归酸酯茶皂甙元A。     

两种清创方法治疗GustiloⅢ型开放性骨折的疗效和卫生经济学观察

目的 比较水动力清创系统清创与常规清创在开放性四肢骨折清创中的效果及经济实用性.方法 采用回顾性队列研究,选择2017年12月—2019年12月空军军医大学第二附属医院骨科收治接受清创植皮或皮瓣治疗的开放性骨折(GustiloⅢ型)患者46例,根据清创方式不同分为水刀清创组(21例)和常规清创组(25例).水刀清创组男...     

腺苷酸活化蛋白激酶在牙周病发生发展中的研究进展

牙周病是以特殊致病菌和破坏性免疫反应相互作用导致的牙周支持组织病理性吸收为特征。腺苷酸活化蛋白激酶（AMPK）作为关键的能量调节因子,通过参与调节重要组织器官脂肪酸和葡萄糖的代谢,从而维持身体内环境的稳态,在代谢性疾病中已被广泛研究。AMPK也可以通过参与牙周骨代谢、免疫反应、基质金属蛋白酶的分泌以及细胞自噬的调节来调控牙周病的发生和发展,在牙周病发病机制中具有潜在作用,并为牙周病的治疗提供了新的治疗靶点。本文对AMPK及其在牙周病发病机制中的研究进展做一综述。     

Acoustic triggered nanobomb for US imaging guided sonodynamic therapy and activating antitumor immunity

We fabricated an ultrasound activated ‘nanobomb’ as a noninvasive and targeted physical therapeutic strategy for sonodynamic therapy and priming cancer immunotherapy. This ‘nanobomb’ was rationally designed via the encapsulation of indocyanine green (ICG) and perfluoropentane (PFP) into cRGD peptide-functionalized nano-liposome. The resulting Lip-ICG-PFP-cRGD nanoparticle linked with cRGD peptide could actively targeted ID8 and TC-1 cells and elicits ROS-mediated apoptosis after triggered by low-intensity focused ultrasound (LIFU). Moreover, the phase change of PFP (from droplets to microbubbles) under LIFU irradiation can produce a large number of microbubbles, which act as intra-tumoral bomber and can detonate explode tumor cells by acoustic cavitation effect. Instant necrosis of tumor cells further induces the release of biologically active damage-associated molecular patterns (DAMPs) to facilitate antitumor immunity. More important, the ‘nanobomb’ in combination with anti-PD-1checkpoint blockade therapy can significantly improve the antitumor efficacy in a subcutaneous model. In addition, the liposomes may also be used as an imaging probe for ultrasound (US) imaging after being irradiated with LIFU. In summary, the US imaging-guided, LIFU activated ROS production and explosion ‘nanobomb’ might significantly improve the antitumor efficacy and overcome drug resistance through combination of SDT and immunotherapy, we believe that this is a promising approach for targeted therapy of solid tumor including ovarian cancer.     

骨保护素/核激活因子受体配体/核激活因子受体(OPG/RANKL/RANK)系统与人工关节置换术后的假体周围骨溶解

人工关节置换术的推广和发展使得多种关节终末期疾病所致的病变获得了良好的临床改善,但术后假体周围骨质溶解这一问题却影响了人工关节远期疗效．长期的研究发现破骨细胞是骨溶解主要原因,而近年研究发现的OPG／RANKL／RANK系统是破骨细胞分化过程中的一个重要信号传导通路,且体内多种激素或因子通过影响骨髓微环境内的OPG／RANKL比率来调节骨代谢．为了给人工关节置换术后骨溶解所致的并发症的防治开辟新的思维,我们综述了OPG／RANKL／RANK系统以及其调控破骨细胞生成、分化对假体周围骨溶解的作用机制．     

强直性脊柱炎的中医康复指导

整理中医药对强直性脊柱炎的辨证施治,以及涉及饮食调养、药膳、中成药、验方、外治法、功能锻炼、日常保健等防治措施。中医药防治强直性脊柱炎,有规范的诊断标准和防治措施,在该病的治疗康复中发挥着重要的作用。     

Drug D,a Diosgenin Derive,Inhibits L-Arginine-Induced Acute Pancreatitis through Meditating GSDMD in the Endoplasmic Reticulum via the TXNIP/HIF-1α Pathway

Acute pancreatitis (AP) is one of the most common causes of hospitalization for gastrointestinal diseases, with high morbidity and mortality. Endoplasmic reticulum stress (ERS) and Gasdermin D (GSDMD) mediate AP, but little is known about their mutual influence on AP. Diosgenin has excellent anti-inflammatory and antioxidant effects. This study investigated whether Diosgenin derivative D (Drug D) inhibits L-arginine-induced acute pancreatitis through meditating GSDMD in the endoplasmic reticulum (ER). Our studies were conducted in a mouse model of L-arginine-induced AP as well as in an in vitro model on mouse pancreatic acinar cells. The GSDMD accumulation in ER was found in this study, which caused ERS of acinar cells. GSDMD inhibitor Disulfiram (DSF) notably decreased the expression of GSDMD in ER and TXNIP/HIF-1α signaling. The molecular docking study indicated that there was a potential interaction between Drug D and GSDMD. Our results showed that Drug D significantly inhibited necrosis of acinar cells dose-dependently, and we also found that Drug D alleviated pancreatic necrosis and systemic inflammation by inhibiting the GSDMD accumulation in the ER of acinar cells via the TXNIP/HIF-1α pathway. Furthermore, the level of p-IRE1α (a marker of ERS) was also down-regulated by Drug D in a dose-dependent manner in AP. We also found that Drug D alleviated TXNIP up-regulation and oxidative stress in AP. Moreover, our results revealed that GSDMD^-/- mitigated AP by inhibiting TXNIP/HIF-1α. Therefore, Drug D, which is extracted from Dioscorea zingiberensis, may inhibit L-arginine-induced AP by meditating GSDMD in the ER by the TXNIP /HIF-1α pathway.