Thermoelectric generators (TEGs) offer notable benefits in harnessing diverse low-grade waste heat from the environment. However, the uninterrupted capture of these energy resources still remains a huge challenge. Herein, we have developed a temperature-adaptive floating thermoelectric generator (TAFTEG) by integrating a temperature-adaptive absorber/emitter (TAA/E) to synergistically exploit renewable energy from the sun, outer space, and the water bodies by leveraging diurnal spectrally selective absorption and nocturnal radiative cooling. The WxV1-xO2-based TAA/E demonstrates remarkably solar absorption of similar to 96 % and a superior switching ability of dynamic thermal radiation modulation from the low emission of similar to 45 % to high emission of similar to 81 %. Assembled with 8 pairs of Bi2Te3-based TEG legs, the TAFTEG enables a stable temperature difference of 34 degrees C under indoor solar irradiation (1 kW m(-2)), yielding a peak power output of similar to 1.0 mW cm(-2), and continuous all-day power supply under both clear and overcast conditions. This strategy paves a new avenue toward the round-the-clock power supply from ambient environments.

Flexible thermoelectric generators can directly convert thermal energy harvested from the human body into electricity. The Ag2Se flexible film, a promising material for wearable thermoelectric generators, normally demonstrates an inferior electrical transport property due to its weakened in-plane mobility. In this study, the in-plane electrical transport properties of flexible Ag2Se films were optimized by alloying with additional sulfur. This optimization is achieved by leveraging the differences in elemental electronegativity and the preferred orientation of the Ag2Se films. The sulfur-alloyed Ag2Se thin film, with a nominal ratio of 3 atom %, can reach a maximum mobility of 1150 cm(-2) V-1 s(-1) at 300 K. So, the optimized room-temperature power factor increases to 1935 mu W m(-1) K-2. Furthermore, the Ag2Se film alloyed with 3 atom % sulfur exhibits excellent flexibility even after 1000 bending cycles with a radius of 5 mm, characterized by a relative resistance increment of less than 3%. In addition, the corresponding pi-type flexible thermoelectric generator possesses a maximum power density of 51 W m(-2) at a temperature difference of 50 K.

Abstract Flexible thermoelectric generators can power wearable electronics by harvesting body heat. However, existing thermoelectric materials rarely realize high flexibility and output properties simultaneously. Here we present a facile, cost-effective, and scalable two-step impregnation method for fabricating a three-dimensional thermoelectric network with excellent elasticity and superior thermoelectric performance. The reticular construction endows this material with ultra-light weight (0.28 g cm−3), ultra-low thermal conductivity (0.04 W m−1 K−1), moderate softness (0.03 MPa), and high elongation (>100%). The obtained network-based flexible thermoelectric generator achieves a pretty high output power of 4 μW cm−2, even comparable to state-of-the-art bulk-based flexible thermoelectric generators.

The clinical experience of Professor Chu Lixi in treating knee osteoarthritis（KOA） is introduced in this article. It is considered that “arthralgia comes earlier than flaccidity” in the development of KOA, with “arthralgia as the manifestation and flaccidity as the root”. The pathogenesis is characterized by “arthralgia developing into flaccidity, coexistence of arthralgia and flaccidity, and mutual impairment between arthralgia and flaccidity”. Professor Chu emphasizes the importance of combining syndrome differentiation-based treatment and stage differentiation-based treatment, giving considerations to the combined treatment of the whole and the local, the manifestations and the root, as well as arthralgia and flaccidity. Meanwhile, the combined use of oral and external treatment of traditional Chinese medicine is highly valued. Therefore, the principles of “combined internal and external treatment” and “one prescription for three uses” are fully practiced. In view of the internal pathogenesis of “imbalance of sinews and bones”, Professor Chu puts “equal emphasis on the treatment of sinews and bones”, advocating combined use of staged orthopaedic manipulative therapies and functional training to achieve “integrated medical treatment and rehabilitation”. One proven case is presented.

Sleep disturbances not only deteriorate Alzheimer’s disease (AD) progress by affecting cognitive states but also accelerate the neuropathological changes of AD. Astrocytes and microglia are the principal players in the regulation of both sleep and AD. We proposed that possible astrocyte-mediated and microglia-mediated neuropathological changes of sleep disturbances linked to AD, such as astrocytic adenosinergic A1, A2, and A3 regulation; astrocytic dopamine and serotonin; astrocyte-mediated proinflammatory status (TNFα); sleep disturbance-attenuated microglial CX3CR1 and P2Y12; microglial Iba-1 and astrocytic glial fibrillary acidic protein (GFAP); and microglia-mediated proinflammatory status (IL-1b, IL-6, IL-10, and TNFα). Furthermore, astrocytic and microglial amyloid beta (Aβ) and tau in AD were reviewed, such as astrocytic Aβ interaction in AD; astrocyte-mediated proinflammation in AD; astrocytic interaction with Aβ in the central nervous system (CNS); astrocytic apolipoprotein E (ApoE)-induced Aβ clearance in AD, as well as microglial Aβ clearance and aggregation in AD; proinflammation-induced microglial Aβ aggregation in AD; microglial-accumulated tau in AD; and microglial ApoE and TREM2 in AD. We reviewed astrocytic and microglial roles in AD and sleep, such as astrocyte/microglial-mediated proinflammation in AD and sleep; astrocytic ApoE in sleep and AD; and accumulated Aβ-triggered synaptic abnormalities in sleep disturbance. This review will provide a possible astrocytic and microglial mechanism of sleep disturbance linked to AD.

痉挛型脑瘫患儿行走时因关节畸形和肌肉挛缩影响，多存在异常运动模式，严重影响患儿的生活质量。重复经颅磁刺激(rTMS)是一项对痉挛型脑瘫患儿有效的辅助治疗方法。本文就rTMS治疗痉挛型脑瘫患儿运动功能的作用和机制做一综述，旨在为临床治疗和研究提供参考和借鉴。

Neural mitochondrial dysfunction, neural oxidative stress, chronic neuroinflammation, toxic protein accumulation, and neural apoptosis are common causes of neurodegeneration. Elamipretide, a small mitochondrially-targeted tetrapeptide, exhibits therapeutic effects and safety in several mitochondria-related diseases. In neurodegeneration, extensive studies have shown that elamipretide enhanced mitochondrial respiration, activated neural mitochondrial biogenesis via mitochondrial biogenesis regulators (PCG-1α and TFAM) and the translocate factors (TOM-20), enhanced mitochondrial fusion (MNF-1, MNF-2, and OPA1), inhibited mitochondrial fission (Fis-1 and Drp-1), as well as increased mitophagy (autophagy of mitochondria). In addition, elamipretide has been shown to attenuate neural oxidative stress (hydrogen peroxide, lipid peroxidation, and ROS), neuroinflammation (TNF, IL-6, COX-2, iNOS, NLRP3, cleaved caspase-1, IL-1β, and IL-18), and toxic protein accumulation (Aβ). Consequently, elamipretide could prevent neural apoptosis (cytochrome c, Bax, caspase 9, and caspase 3) and enhance neural pro-survival (Bcl2, BDNF, and TrkB) in neurodegeneration. These findings suggest that elamipretide may prevent the progressive development of neurodegenerative diseases via enhancing mitochondrial respiration, mitochondrial biogenesis, mitochondrial fusion, and neural pro-survival pathway, as well as inhibiting mitochondrial fission, oxidative stress, neuroinflammation, toxic protein accumulation, and neural apoptosis. Elamipretide or mitochondrially-targeted peptide might be a targeted agent to attenuate neurodegenerative progression.

Objective Cardiac mitochondrial dysfunction was found in ischemic heart disease (IHD). Hence, this study determined the effects of exercise training (ET) on cardiac mitochondrial respiration and cardiac mitochondrial quality control in IHD. Methods A narrative synthesis was conducted after searching animal studies written in English in three databases (PubMed, Web of Science, and EMBASE) until December 2020. Studies that used aerobic exercise as an intervention for at least 3 weeks and had at least normal, negative (sedentary IHD), and positive (exercise-trained IHD) groups were included. The CAMARADES checklist was used to check the quality of the included studies. Results The 10 included studies (CAMARADES score: 6–7/10) used swimming or treadmill exercise for 3–8 weeks. Seven studies showed that ET ameliorated cardiac mitochondrial respiratory function as manifested by decreased reactive oxygen species (ROS) production and increased complexes I-V activity, superoxide dismutase 2 (SOD2), respiratory control ratio (RCR), NADH dehydrogenase subunits 1 and 6 (ND1/6), Cytochrome B (CytB), and adenosine triphosphate (ATP) production. Ten studies showed that ET improved cardiac mitochondrial quality control in IHD as manifested by enhanced and/or controlled mitochondrial biogenesis, dynamics, and mitophagy. Four other studies showed that ET resulted in better cardiac mitochondrial physiological characteristics. Conclusion Exercise training could improve cardiac mitochondrial functions, including respiration, biogenesis, dynamics, and mitophagy in IHD. Systematic review registration https://www.crd.york.ac.uk/prospero/ display_record.php?RecordID=226817 , identifier: CRD42021226817.

Exploring the spectrally selective absorbers with high optical performance and excellent thermal stability is crucial to improve the conversion efficiency of solar energy to electricity in concentrated solar power (CSP) systems. However, there are limited reports on the selective solar absorbers utilized at 900 o C or above. Herein, we developed a selective absorption coating based on the ultra-high temperature ceramic ZrC and the quasi-optical microcavity (QOM) optical structure, and experimentally achieved the absorber via depositing an all-ceramic multilayer films on a stainless steel substrate by magnetron sputtering. The prepared multi-layer selective absorber demonstrates an excellent high solar absorptance of ∼0.964 due to the multi absorptance mechanisms in the QOM, and a relatively low thermal emittance of ∼0.16 (82°C). Moreover, the coating can survive at 900 o C in vacuum for 100 h with a superior spectral selectivity of 0.96/0.143 (82°C) upon annealing, resulting from the introduction of ultra-high temperature ceramic ZrC in the QOM structure. Under the conditions of a stable operating temperature of 900°C and a concentration ratio of 1,000 suns, the calculated ideal conversion efficiency using this absorber can reach around 68%, exceeding most solar selective absorbers in previous reports.

This systematic review sought to determine the effects of Mitochondrial division inhibitor-1 (Mdivi-1) on neural mitochondrial dysfunction and neural mitochondria-mediated apoptosis in ischemia/reperfusion (I/R) injury after ischemic stroke. Pubmed, Web of Science, and EMBASE databases were searched through July 2021. The studies published in English language that mentioned the effects of Mdivi-1 on neural mitochondrial dysfunction and neural mitochondria-mediated apoptosis in I/R-induced brain injury were included. The CAMARADES checklist (for in vivo studies) and the TOXRTOOL checklist (for in vitro studies) were used for study quality evaluation. Twelve studies were included (median CAMARADES score = 6; TOXRTOOL scores ranging from 16 to 18). All studies investigated neural mitochondrial functions, providing that Mdivi-1 attenuated the mitochondrial membrane potential dissipation, ATP depletion, and complexes I-V abnormalities; enhanced mitochondrial biogenesis, as well as inactivated mitochondrial fission and mitophagy in I/R-induced brain injury. Ten studies analyzed neural mitochondria-mediated apoptosis, showing that Mdivi-1 decreased the levels of mitochondria-mediated proapoptotic factors (AIF, Bax, cytochrome c, caspase-9, and caspase-3) and enhanced the level of antiapoptotic factor (Bcl-2) against I/R-induced brain injury. The findings suggest that Mdivi-1 can protect neural mitochondrial functions, thereby attenuating neural mitochondria-mediated apoptosis in I/R-induced brain injury. Our review supports Mdivi-1 as a potential therapeutic compound to reduce brain damage in ischemic stroke (PROSPERO protocol registration ID: CRD42020205808).Systematic Review Registration: [https://www.crd.york.ac.uk/prospero/], identifier [CRD42020205808].

Exploiting renewable energy is an extremely effective strategy for alleviating and addressing the energy issues. To effectively harvest renewable energy, the investigations of fundamental thermodynamics resources of the sun and outer space have attracted significant attentions and various attempts have been carried out for energy-related applications. The key of effective energy harvesting and conserving from the sun and outer space relies on the precise manipulation of the electromagnetic responses including selective reflection, transmission, and absorption/emission in particular frequency ranges, which plays a critical role in various practical applications. According to the utilization of spectral bands, the electromagnetic responses are summarized into the single-band and multi-band characteristics. The single band applications including the photovoltaic and photothermal conversion, thermal photons radiation, radiation cooling, and smart windows coatings, enable individually the utilization of the solar energy or the thermal radiation. In addition, the hybrid photovoltaic-thermal system and solar absorber/thermal emitter subtly synergize the photovoltaic and photothermal or thermal radiation through multi-band spectral modulation. In order to figure out the basic mechanisms of existing renewable energy technologies based on various electromagnetic responses, herein, we briefly summarize the optical characteristics from the perspective of spectral tuning and review their corresponding practical technologies. This article aims to provide a perspicuous mainline for existing spectral controlling work and to inspire other innovative optical tuning for potential energy applications. (C) 2021 Elsevier Ltd. All rights reserved.

The anti-apoptotic and pro-survival effects of exercise training were evaluated on the early aged hypertensive rat cerebral cortex. The brain tissues were analysed from ten sedentary male Wistar Kyoto normotensive rats (WKY), ten sedentary spontaneously 12 month early aged hypertensive rats (SHR), and ten hypertensive rats undergoing treadmill exercise training (60 min/day, 5 days/week) for 12 weeks (SHR-EX). TUNEL-positive apoptotic cells, the expression levels of endonuclease G (EndoG) and apoptosis-inducing factor (AIF) (caspase-independent apoptotic pathway), Fas ligand, Fas death receptor, tumor necrosis factor (TNF)-α, TNF receptor 1, Fas-associated death domain, active caspase-8 and active caspase-3 (Fas-mediated apoptotic pathways) as well as t-Bid, Bax, Bak, Bad, cytochrome c, active caspase 9 and active caspase-3 (mitochondria-mediated apoptotic pathways) were reduced in SHR-EX compared with SHR. Pro-survival Bcl2, Bcl-xL, p-Bad, 14-3-3, insulin-like growth factor (IGF)-1, pPI3K/PI3K, and pAKT/AKT were significantly increased in SHR-EX compared to those in SHR. Exercise training suppressed neural EndoG/AIF-related caspase-independent, Fas/FasL-mediated caspase-dependent, mitochondria-mediated caspase-dependent apoptotic pathways as well as enhanced Bcl-2 family-related and IGF-1-related pro-survival pathways in the early aged hypertensive cerebral cortex. These findings indicated new therapeutic effects of exercise training on preventing early aged hypertension-induced neural apoptosis in cerebral cortex.

Skeletal muscle injuries can cause significant change in the ultrastructure and the metabolism of the skeletal muscle cells. Observation of the ultrastructure and measurements of the metabolism biomarkers such as total superoxide dismutase (T-SOD), malondialdehyde (MDA), and creatine kinase (CK) can be used to evaluate the degree of damage in human skeletal muscle injury. Rolling manipulation is the most popular myofascial release technique in Traditional Chinese Medicine. This study aimed to investigate the effects of intermittent pressure imitating rolling manipulation (IPIRM) of Traditional Chinese Medicine on ultrastructure and metabolism in the injured HSKMCs. Methods: In vitro techniques were used to culture HSKMCs, which were injured with high doses of dexamethasone sodium phosphate. Cells were divided into four groups-control normal group (CNG), control injured group (CIG), rolling manipulation group (RMG), and sine pressure group (SPG). RMG and SPG cells were cyclically exposed to 3.0 Kg (6.6 Pounds) of maximum force at a frequency of 2.0 Hz for 10 min in the Flexcell compression system for duration of 3 days continually. The cell ultrastructure, total superoxide dismutase (T-SOD) activity, malondialdehyde (MDA) content, and creatine kinase (CK) activity of the groups were assessed. Conclusion: These results suggest that the mechanical effects of rolling manipulation in TCM could not only improve the recovery of injured skeletal muscle cells by ameliorating organelles arrangement, reducing organelle swelling, and maintaining nuclear membrane integrity, but also ameliorate the functions of cellular metabolism by increasing T-SOD activity and decreasing MDA content and CK activity in injured skeletal muscle. Then the Hippo/Yap signal pathway was detected, and the proteins in each group were detected by Western Blot. The protein expression of upstream protein p-LATS1 and downstream protein p-Yap (Ser127) in each group was observed to explore the biomechanical mechanism of the method. The relative protein expression of p-LATS1 and p-Yap in (RMG) group was significantly higher than that in injured (CIG) group (P < 0.05). It was suggested that Hippo/Yap pathway was related to the stimulation of 3D human skeletal muscle cells, and the proliferation pathway of 3D human skeletal muscle cells could be opened by stimulation of three dimensional human skeletal muscle cells. It may be one of the biological mechanisms caused by the mechanical effects of manipulations in TCM.

Osteoarthritis (OA) is frequently associated with loss of articular cartilage and is more common in elderly patients. Progranulin (PGRN) is a chondrogenic factor. However, the role of PGRN in inflammatory articular chondrocyte arthritis and related mechanisms has not been elucidated. In vitro cultured chondrocytes were divided into control group, LPS group that was treated with 1 μg/ml lipopolysaccharide (LPS), and PGRN group, in which LPS-stimulated chondrocytes were treated with PGRN (5 μM and 10 μM). The survival rate of chondrocytes was detected by tetrazolium salt colorimetry (MTT method). MMP-3, tissue metalloproteinase inhibitor 1 (TIMP-1), and MMP-3/TIMP-1 ratio were assessed by Western blot. The expressions of FAK and MAPK were detected by Western blot. TNF-α and IL-β secretion was evaluated by ELISA. Chondrocyte survival rate was decreased, Caspase 3 activity increased, MMP-3 expression upregulated, TIMP-1 expression reduced, MMP-3/TIMP-1 ratio elevated, FAK and MAPK expressions downregulated, and TNF-α and IL-1β secretions enhanced in LPS group (P < 0.05). PGRN significantly promoted the survival of LPS-treated chondrocytes, attenuated Caspase 3 activity, decreased MMP-3 level, enhanced TIMP-1 level, decreased MMP-3/TIMP-1 ratio, upregulated FAK and MAPK, and inhibited TNF-α and IL-1β secretions dose dependently (P < 0.05). PGRN can reduce the apoptosis of osteoarthritic chondrocytes, promote cell proliferation, reduce secretion of inflammatory factors, and delay the progression of osteoarthritis possibly through regulating FAK/MAPK pathway.

2019年12月以来,新型冠状病毒肺炎(简称“新冠肺炎”)在武汉暴发并迅速传播至全国,给患者的生命安全和中国社会经济等带来严重损害.为防止新冠肺炎患者长时间卧床、缺乏活动带来的并发症以及对心肺功能和身心状态的不利影响,促进患者肺功能恢复并改善预后结局,上海中医药大学康复医学团队依据现有的新冠肺炎相关诊疗指导意见,在负责一线诊治新冠肺炎的上海市公共卫生临床中心专家的提议和指导下,提出了针对轻型和重型新冠肺炎恢复期患者的康复训练指导建议.轻型患者建议习练健身气功养肺方,重型患者建议进行床上康复训练.希望此建议有助于全国一线负责新冠肺炎诊治的医疗同道对患者进行因人制宜的指导,促进广大患者早日康复.

目的 探讨淫羊藿苷(icariin,ICA)对软骨细胞增殖功能的影响及其作用机制.方法 选取SD大鼠四肢长骨进行关节软骨细胞的分离与培养,将第二代细胞接种至96孔板或6孔板进行培养,并将其随机分为对照组、低剂量组、中剂量组和高剂量组,对照组软骨细胞采用常规培养基培养,低剂量组、中剂量组和高剂量组软骨细胞分别在常规培养基础上添加0.1、1、10μmol/L的ICA,干预1、3、5 d后采用MTT法与流式细胞术分别检测四组软骨细胞的增殖和凋亡情况,并通过实时荧光定量聚合酶链反应分析ICA干预5 d后Wnt/β-catenin通路相关基因的表达水平.结果 ICA干预1 d后,四组软骨细胞在450 nm波长处的吸光度(optical density 450,OD450)与凋亡率比较差异均无统计学意义(均P>0.05).ICA干预3 d后,中剂量组、高剂量组软骨细胞的OD450均显著高于对照组(均P<0.05),凋亡率均显著低于对照组(均P<0.05),而低剂量组与对照组软骨细胞的OD450比较差异无统计学意义(P>0.05).ICA干预5 d后,低剂量组、中剂量组和高剂量组软骨细胞的OD450均显著高于对照组(均P<0.05),凋亡率均显著低于对照组(均P<0.05).低剂量组、中剂量组和高剂量组软骨细胞的Wnt2、β-catenin、CCND1相对表达水平均显著高于对照组(均P<0.05).结论 ICA能通过促进Wnt/β-catenin信号通路而促进软骨细胞的增殖,抑制细胞凋亡,且呈剂量、时间依赖性.

目的:研究Flexcell-5000(Fx-5000)细胞压力加载装置模拟推拿(滚)法样刺激不同压力值对骨骼肌细胞肌酸激酶(CK)的影响.方法:培养人体骨骼肌细胞,利用地塞米松建立人体骨骼肌细胞损伤模型.将正常细胞和损伤细胞各自分为空白组和不同压力加载组:A力组(l0Kpa),B力组(5Kpa),C力组(1.5Kpa).通过FX-5000细胞力学加载装置模拟(滚)法曲线,对压力加载组细胞进行相应的力学加载,持续3d,每次10min,然后对各组细胞的CK值进行检测.结果:与正常细胞空白组比较,损伤细胞空白组的CK值显著增高(P＜0.05);与损伤细胞空白组比较,损伤细胞C力组的CK值显著降低(P＜0.05).结论:FX-5000模拟推拿(滚)法曲线1.5Kpa压力对于降低损伤骨骼肌细胞肌酸激酶的作用要优于5Kpa压力和10Kpa压力;有助于进一步研究(滚)法刺激对于骨骼肌细胞的作用机制.

目的 观察中医手法对实验性兔膝骨关节炎软骨退变的干预作用,并从细胞信号转导角度探讨其作用机制.方法 24只新西兰大白兔随机分为3组,即正常组、模型组和手法组,除正常组外,其余两组动物均采用手术方法建立膝骨关节炎模型.造模4周后对手法组给予髌骨按揉、关节被动屈伸等形式的手法治疗.干预8周后处死动物,暴露膝关节行形态学观察,并取股骨髁部做病理切片,行HE染色,镜下观察其组织病理学特征并进行Mankin's评分,比较各组关节软骨退变情况.应用RT-PCR方法分别检测滑膜组织中IL-1β、iNOS、MMP-13和软骨组织中P38、ERK1/2的mRNA表达水平.应用Western blot方法检测软骨组织内MMP-13及磷酸化的ERK1/2(p-ERK1/2)的蛋白表达.比较各组实验数据并进行统计学分析.结果 手法组关节软骨退变程度较模型组明显减轻,Mankin's评分分值显著低于模型组(P＜0.05).手法组软骨P38、ERK1/2及滑膜组织IL-1β、iNOS、MMP-13的mRNA表达水平较模型组显著下调(P＜0.05).模型组和手法组的MMP-13、p-ERK1/2的蛋白表达较正常关节软骨明显增强,而手法组MMP-13、p-ERK1/2的蛋白活化程度与模型组比较明显受到抑制.结论 中医手法能够有效抑制膝骨关节炎的软骨退变程度,影响炎症介质和细胞因子的表达,其机制可能是通过抑制软骨MAPK信号转导通路发挥作用.

Objective To investigate the effects of icariin (ICA) on the phenotype of interleukin-1 β (IL-1β)-induced inflammatory chondrocytes.Methods The articular chondrocytes of rats were isolated and cultured.The primary chondrocytes were induced by IL-1β,and the inflammatory environment of chondrocytes in osteoarthritis was simulated.The cells were divided into the blank group,model group (treated with IL-1β at concentration of 10 mg/L),ICA group with lowconcentration (treated with IL-1β at concentration of 10 mg/L and ICA at concentration of 1 μmol/L)and ICA group with high-concentration(treated with IL-1β at concentration of 10 mg/L and ICA at concentration of 5 μmol/L).The protein expressions of collagen-Ⅱf and aggrecan were detected by Western blot.The mRNA expressions of collagen-Ⅱ,aggrecan,matrix metallopeptidase-13 (MMP-13) and a disintegrin and metalloprotease with thrombospondin motifs-5 (ADAMTS-5) were detected by RT-PCR.Results After the cells were cuhured for three day,compared with the model group,ICA could obviously promote the mRNA and protein expressions of collagen-Ⅱ in the inflammatory chondrocytes(P＜0.05);and this effect in the ICA group with high-concentration was more significant than that in the ICA group with low-concentration(P＜0.05).Compared with the model group,ICA could obviously promote the mRNA and protein expressions of aggrecan in the inflammatory chondrocytes(P＜0.05);and this effect shows no obviously difference between the low-and high-concentration.Compared with the model group,ICA could inhibit the mRNA expressions of MMP-13 and ADAMTS-5(P＜0.05),and the inhibiting effect on MMP-13 mRNA expression was more significant in the ICA group with high-concentration (P ＜ 0.05);there was no obvious difference on the ADAMTS-5 mRNA expression between the low-and high-concentration.Conclusion ICA can inhibit the expressions of MMP-13 and ADAMTS-5 and promote the expressions of collagen-Ⅱ and aggrecan in the inflammatory chondrocytes,and thus maintain the chondrocytes phenotype and promote the matrix metabolism.

Objective To investigate the effect of icariin(ICA)on IL-1β-induced chondrocytes degeneration. Methods Primary chondrocytes isolated from articular cartilage of newborn rats were cultured in vitro and treated with icariin at 1×10-7, 1×10-6and 1×10-5mol/L. The cell proliferation was measured by MTT at 12, 24, 36, 48, 60 and 72 h. The cultured rat chondrocytes were than dividing into control group(N group), IL-1β-stimulated group(M group treated with IL-1β 10 ng/ml), ICA-L(1×10-7mol/L)and ICA-H(1×10-6mol/L)groups(IL-1β-stimulated cells treated with ICA). The concentrations of collagen-Ⅱ and glycosaminoglycan(GAG)in culture media after 72 h of intervention were determined by ELISA and the expressions of Col-Ⅱ,MMP13,Acan,Sox9 mRNA were detected by RT-PCR. Results 1×10-5mol/L ICA inhibited chondrocytes proliferation when intervened for 24 h,while promoted cell proliferation after 72 h;there was no significant difference between groups with and without ICA at 48 h or 60 h.ICA concentration at 1×10-7mol/L and 1×10-6mol/L both significantly promoted cell proliferation from 36 h to 72 h, but ICA at 1×10-7mol/L had no significant effect at 60 h.ICA at both concentration of 1×10-7mol/L and 1×10-6mol/L increased the GAG level in culture supernatant,but there was no significant change in Col-Ⅱlevel in ICA-H group. Compared with M group, the expression of Acan/Sox9 mRNA in ICA-L group and Col-ⅡmRNA in ICA-H group significantly went up,while MMP13 decreased in ICA-H group. Conclusion Icariin can affect the matrix microenvironment of chondrocytes, promote the phenotype gene expression and inhibit MMP13 mRNA expression,and further protects chondrocytes from IL-1β-induced degeneration.