Surface barriers to mass transfer in nanoporous materials for catalysis and separations.

Surface barriers to mass transfer in various nanoporous materials have been increasingly identified. These past few years especially, a significant impact on catalysis and separations has come to light. Broadly speaking, there are two types of barriers: internal barriers, which affect intraparticle diffusion, and external barriers, which determine the uptake and release rates of molecules into and out of the material. Here, we review the literature on surface barriers to mass transfer in nanoporous materials and describe how the existence and influence of surface barriers has been characterized, aided by molecular simulations and experimental measurements. As this is a complex, evolving research topic, without consensus from the scientific community at the time of writing, we present various current viewpoints, not always in agreement, on the origin, nature, and function of such barriers in catalysis and separation. We also emphasize the need for considering all the elementary steps of the mass transfer process in optimally designing new nanoporous and hierarchically structured adsorbents and catalysts.

Effect of External Surface Diffusion Barriers on Platinum/Beta-Catalyzed Isomerization of n-Pentane.

We have developed a generalizable strategy to quantify the effect of surface barriers on zeolite catalysis. Isomerization of n-pentane, catalyzed by Pt/Beta, is taken as a model reaction system. Firstly, the surface modification by chemical liquid deposition of SiO2 was carried out to control the surface barriers on zeolite Beta crystals. The deposition of SiO2 leads to a very slight change in the physical properties of Beta crystals, but an obvious reduction in Brønsted acid sites. Diffusion measurements by the zero-length column (ZLC) method show that the apparent diffusivity of n-pentane can be more than doubled after SiO2 deposition, indicating that the surface barriers have been weakened. Catalytic performance was tested in a fixed-bed reactor, showing that the apparent catalytic activity improved by 51-131 % after SiO2 deposition. These results provide direct proof that reducing surface barriers can be an effective route to improve zeolite catalyst performance deteriorated by transport limitations.

Understanding the Role of Internal Diffusion Barriers in Pt/Beta Zeolite Catalyzed Isomerization of n-Heptane.

Applications of zeolites in catalysis are plagued by strong diffusion resistance, which results from limitations to molecular transport in micropores, across external crystal surfaces, but also across internal interfaces. The first type of diffusion resistance is well understood, the second is receiving increasing attention, while the diffusion barriers at internal interfaces remain largely unclear. We take Pt/Beta catalyzed isomerization of n-heptane as the model system to explore the role of internal diffusion barriers in zeolite catalysis. The two as-synthesized Pt/Beta catalysts have an identical Pt loading, similar Beta particle size and acidity, but different internal structures. A Pt/Beta crystal with no observable internal interfaces can be 180 % higher in activity and 22 % higher in selectivity than its counterpart with numerous internal interfaces. This can only be attributed to the strong transport barriers across internal interfaces, as supported by directly comparing the apparent diffusivities of the two Beta samples.

Detection of RAGE expression and its application to diabetic wound age estimation.

With the prevalence of diabetes, it is becoming important to analyze the diabetic wound age in forensic practice. The present study investigated the time-dependent expression of receptor for advanced glycation end products (RAGE) during diabetic wound healing in mice and its applicability to wound age determination by immunohistochemistry, double immunofluorescence, and Western blotting. After an incision was created in genetically diabetic db/db mice and control mice, mice were killed at posttraumatic intervals ranging from 6 h to 14 days, followed by the sampling of wound margin. Compared with control mice, diabetic mice showed the delayed wound healing. In control and diabetic wound specimens, RAGE immunoreactivity was observed in a small number of polymorphonuclear cells (PMNs), a number of macrophages, and fibroblasts. Morphometrically, the positive ratios of RAGE in macrophages or fibroblasts considerably increased in diabetic wounds during late repair, which exceeded 60% at 7 and 10 days post-injury. There were no control wound specimens to show a ratio of >60% in macrophages or fibroblasts. By Western blotting analysis, the ratios of RAGE to GAPDH were >1.4 in all diabetic wound samples from 7 to 10 days post-injury, which were >1.8 at 10 days after injury. By comparison, no control wound specimens indicated a ratio of >1.4. In conclusion, the expression of RAGE is upregulated and temporally distributed in macrophages and fibroblasts during diabetic wound healing, which might be closely involved in prolonged inflammation and deficient healing. Moreover, RAGE is promising as a useful marker for diabetic wound age determination.

The time-dependent expression of α7nAChR during skeletal muscle wound healing in rats.

The study on time-dependent expression of α7 nicotine acetylcholine receptor (α7nAChR) was performed by immunohistochemistry, Western blotting, and real-time PCR during skeletal muscle wound healing in rats. Furthermore, co-localization of α7nAChR with macrophage or myofibroblast marker was detected by double immunofluorescence. A total of 50 Sprague-Dawley male rats were divided into control and contusion groups (3 h, 6 h, 12 h, 1 day, 3 days, 5 days, 7 days, 10 days, and 14 days post-injury). In the uninjured controls, α7nAChR positive staining was observed in the sarcolemma and sarcoplasm of normal myofibers. In wounded specimens, a small number of polymorphonuclear cells, a number of macrophages and myofibroblasts showed positive reaction for α7nAChR in contused zones. Morphometrically, the average ratios of α7nAChR-positive cells were over 50 % from 3 to 10 days after contusion, and exceeded 60 % at 5 and 7 days post-injury. Besides, the positive ratios of α7nAChR were <50 % at the other posttraumatic intervals. By Western blotting analysis, the average ratio of α7nAChR protein expression maximized at 7 days after injury, which was >2.13. Similarly, the relative quantity of α7nAChR mRNA expression peaked at 7 days post-wounding as compared with control by real-time PCR detection, showing a relative quantity of >2.65. In conclusion, the expression of α7nAChR is upregulated and temporally distributed in macrophages and myofibroblasts during skeletal muscle wound healing, which might be closely involved in inflammatory response and fibrotic repair after injury. Moreover, α7nAChR is promising as a useful marker for wound age determination of skeletal muscle.

[The contributing risk factors, prevention and treatment of functional dependence among the oldest-old and elderly subjects].

OBJECTIVE: To compare the risk factors on the functional dependence between the oldest-old and elderly veterans. METHODS: A cross-sectional survey was conducted among veterans ( ≥ 60 years of age) lived in 44 veterans' communities in Beijing. The socio-demographic information and history of non-communicable chronic diseases were collected via face-to-face interviews, and the functional status was assessed by the 20-item version of the Activities of Daily Living Scale. RESULTS: The risk factors associated with increased hazard of the functional dependence in the oldest-old ( ≥ 80 years old) were cognitive impairment, extrapyramidal diseases, cerebral infarction, transient ischemic attack, sleep disorders, hypnotics, osteoarthrosis, hypertension and fall with the odds ratio (OR) of 1.241-2.962 (all P < 0.05). Stroke, depression, cognitive impairment, extrapyramidal diseases, sleep disorders, hypnotics, fall, cardiovascular diseases, osteoarthrosis and hearing loss were the risk factors for that in the elderly subjects (aged 60-79 years). The OR was 1.232-5.790 (all P < 0.05). However, avocational activities such as social activity, physical exercise, photography, reading and games, decreased the risk of functional dependence in both the oldest-old and elderly people. CONCLUSIONS: Neuropsychiatric disorders are the leading causes contributed to the functional dependence among oldest-old and elderly population. Neurodegenerative diseases in the oldest-old, stroke and depression in elderly people should be the priorities in ameliorating disability. Healthy lifestyle and avocational activities could improve the functional status of the oldest-old and elderly population.

[Protective effect of qingxin kaiqiao fang containing cerebrospinal fluid on PC12 cell injury induced by Abeta25-35].

OBJECTIVE: To observe the protective effect of Qingxin Kaiqiao Fang containing cerebrospinal fluid on PC12 cell injury induced by Abeta25-35, in order to provide basis for clinical application of the formula. METHOD: Sprague Dawley rats were orally administration with Qingxin Kaiqiao Fang (7.9 g x kg(-1)) twice a day for 3.5 days to prepare Qingxin Kaiqiao Fang containing cerebrospinal fluid. The nerve cell injury model was established by PC12 cells and Abeta25-35 with the concentration of 10 micromol x L(-1). The expressions of Bax, Bcl-2 and Caspase-3 mRNA were detected by immunohistochemical method in the PC12 cells. RESULT: The Qingxin Kaiqiao Fang group showed a significant higher PC12 cell activity than the model group, with decrease in Bax mRNA and Caspase-3 mRNA expressions and increase in Bcl-2 mRNA expression. There was a significant difference from the model group (P < 0.05, P < 0.01). CONCLUSION: Qinxin Kaiqiao Fang shows a significant protective effect on Abeta25-35-induced nerve cell injury.

[Effects of α-lipoic acid and vitamin C on oxidative stress in rat exposed to chronic arsenic toxicity].

OBJECTIVE: To explore arsenic-induced oxidative stress and the protective efficacy of α-lipoic acid and vitamin c. METHODS: 50 male SD rats were randomly divided into 5 groups. Ten rats (the control group) were exposed to deionized water for 6 weeks, and the others were alone exposed to sodium arsenite (50 mg/L water) for 6 weeks, at the same time, three group rats were administered intragastrically (i.g.) with α-lipoic acid 10 mg×kg(-1)×d(-1) and vitamin C 25 mg×kg(-1)×d(-1) either alone or in combination. At the end of experiment, blood was drawn from abdominal aorta, and then the blood, brain and liver of rats were used for biochemical assays, including blood glutathione (GSH), δ-aminolevulinic acid dehydratase (δ-ALAD ), reactive oxygen species (ROS) and oxidized glutathione (GSSG) level. At the same time, the super oxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, catalase (CAT) activity, ATPase activity of brain and liver were determined. The caspase activity of brain were also determined. RESULTS: There were a significant increase in ROS level (P < 0.05), but a significant decrease in δ-ALAD activity (P < 0.01) in the chronic arsenic toxicity model group compared with the control group. These alterations were marginally restored by co-administration of vitamin C and α-lipoic acid individually, while significant recovery was observed in the animals supplemented with both the antioxidants together with arsenite in rat (P < 0.05). At the same time, there was a significant increase in the ROS and TBARS level of the brain and liver (P < 0.05), and caspase activity of the brain (P < 0.05), while there was a significant decrease in antioxidant enzymes and ATPase activity on arsenite exposure in rats (P < 0.05). These alterations were also marginally restored by co-administration of vitamin C and α-lipoic acid individually, while significant recovery was observed in the animals supplemented with both the antioxidants together with arsenite in rat (P < 0.05). CONCLUSIONS: Arsenite-induced oxidative stress can be significantly protected by co-administration of α-lipoic acid and vitamin C individually, but the best effects could be observed with combined administration of two antioxidants during arsenite exposure in animals. The dietary intervention of or supplementation with natural dietary nutrients is possible to prevent the effects of arsenic in populations of risk.

IL-33 Alleviated Brain Damage via Anti-apoptosis, Endoplasmic Reticulum Stress, and Inflammation After Epilepsy.

Interleukin (IL)-33 belongs to a novel chromatin-associated cytokine newly recognized by the IL-1 family, and its specific receptor is the orphan IL-1 receptor (ST2). Cumulative evidence suggests that IL-33 plays a crucial effect on the pathological changes and pathogenesis of central nervous system (CNS) diseases and injuries, such as recurrent neonatal seizures (RNS). However, the specific roles of IL-33 and its related molecular mechanisms in RNS remain confused. In the present study, we investigated the protein expression changes and co-localized cell types of IL-33 or ST2, as well as the effect of IL-33 on RNS-induced neurobehavioral defects, weight loss, and apoptosis. Moreover, an inhibitor of IL-33, anti-IL-33 was performed to further exploited underlying mechanisms. We found that administration of IL-33 up-regulated the expression levels of IL-33 and ST2, and increased the number of its co-localization with Olig-2-positive oligodendrocytes and NeuN-positive neurons at 72 h post-RNS. Noteworthily, RNS-induced neurobehavioral deficits, bodyweight loss, and spatial learning and memory impairment, as well as cell apoptosis, were reversed by IL-33 pretreatment. Additionally, the increase in IL-1ß and TNF-α levels, up-regulation of ER stress, as well as a decrease in anti-apoptotic protein Bcl-2 and an increase in pro-apoptotic protein CC-3 induced by RNS are prevented by administration of IL-33. Moreover, IL-33 in combination with Anti-IL-33 significantly inverted the effects of IL-33 or Anti-IL-33 alone on apoptosis, ER stress, and inflammation. Collectively, these data suggest that IL-33 attenuates RNS-induced neurobehavioral disorders, bodyweight loss, and spatial learning and memory deficits, at least in part through mechanisms involved in inhibition of apoptosis, ER stress, and neuro-inflammation.

[Analysis of 90 autopsy cases in medical legal dispute].

OBJECTIVE: To analyze the significance of forensic autopsy in medical tangle. METHODS: Ninety autopsy cases of medical legal dispute were retrospectively analyzed from the database of our department from 2001 to 2008. All cases were analyzed and classified based on age, sex, cause of death, clinic diagnosis and forensic diagnosis. RESULTS: The age ranged from 1 day to 72 years, and the ratios of male to female is 1:1. The most common healthcare facilities involved were county hospitals (30 cases, 33.33%). The coincidence rate between clinical diagnoses and pathological diagnoses was 33.33%. CONCLUSION: The forensic autopsy is valuable to solve or even avoid the occurrence of medical legal dispute.

[Effects of curcumin on malondialdehyde and c-fos protein in hypoxia ischemia brain tissue in rats].

OBJECTIVE: To explore the effects of curcumin on the content of malondialdehyde (MDA) and the expression level of c-fos protein following hypoxia ischemia brain damage (HIBD) in rats. METHODS: Sprague-Dauley (SD) rats were randomly divided into four groups as the following: sham group, hypoxia ischemia brain damage group, curcumin group and solvent control group. The content of MDA in the brain was measured by colorimetry. The expression level of c-fos protein in the cortex tissue was detected by immunohistochemistry. Morphologic and structural changes of neuron cells of the cortex were observed by electron microscopy. RESULTS: The content of MDA was clearly lower in curcumin group than that in the other groups at the same time after HIBD. The expression level of c-fos protein was higher in the curcumin group than that in the other groups (P<0.05). Electron microscopy showed that the morphologic and structural changes of neuron cells of cortex in the curcumin group were reduced. CONCLUSION: Curcumin could significantly decrease the content of MDA, increase the expression level of c-fos protein and reduce the damage of the neuron cells.

Balancing the Micro-Mesoporosity for Activity Maximization of N-Doped Carbonaceous Electrocatalysts for the Oxygen Reduction Reaction.

Carbonaceous porous structures have instigated global research interest as promising low-cost electrocatalysts for numerous energy technologies. However, the rational design principle of pore structures for activity maximization is still unclear. In this work, a series of N-doped carbon (N-C) catalysts with exclusively different micro-mesoporosity are investigated for the oxygen reduction reaction (ORR). By combining the experiment results and a pioneering mathematical model, it was observed that the best catalytic activity can only be attained by balancing the micro-mesoporosity. These findings offer a definite criterion for pore structure optimization in carbon-based ORR catalysts, which is of great importance for various energy technologies.

[Acute necrotizing pancreatitis and postmortem autolysis of pancreas].

OBJECTIVE: To compare the pathomorphologic changes between the pancreas in acute necrotizing pancreatitis (ANP) and that in acute deaths of rats (within 48 hours) so as to find the distinctions. METHODS: The animal models of ANP and other acute deaths (electroshock, mechanic asphyxia/strangle, and acute poisoning with tetramine) were established according to the criteria. Half-quantitative grading and image quantitative analysis methods were employed to observe the gross and microscopic changes of the pancreases. RESULTS: Three features including inflammation infiltrate, fat necrosis and calcium deposit in the ANP group were considerably different from that in other acutely died rat group (P<0.05). CONCLUSION: Inflammation infiltrate, fat necrosis and calcium deposit are the most important pathologic features found in ANP by common light microscope, distinguishing ANP from postmortem pancreatic autolysis.

IL-33/ST2L Signaling Provides Neuroprotection Through Inhibiting Autophagy, Endoplasmic Reticulum Stress, and Apoptosis in a Mouse Model of Traumatic Brain Injury.

Interleukin-33 (IL-33) is a member of the interleukin-1 (IL-1) cytokine family and an extracellular ligand for the orphan IL-1 receptor ST2. Accumulated evidence shows that the IL-33/ST2 axis plays a crucial role in the pathogenesis of central nervous system (CNS) diseases and injury, including traumatic brain injury (TBI). However, the roles and molecular mechanisms of the IL-33/ST2 axis after TBI remain poorly understood. In this study, we investigated the role of IL-33/ST2 signaling in mouse TBI-induced brain edema and neurobehavioral deficits, and further exploited underlying mechanisms, using salubrinal (SAL), the endoplasmic reticulum (ER) stress inhibitor and anti-ST2L. The increase in IL-33 level and the decrease in ST2L level at injured cortex were first observed at 24 h post-TBI. By immunofluorescent double-labeled staining, IL-33 co-localized in GFAP-positive astrocytes, and Olig-2-positive oligodendrocytes, and predominantly presented in their nucleus. Additionally, TBI-induced brain water content, motor function outcome, and spatial learning and memory deficits were alleviated by IL-33 treatment. Moreover, IL-33 and SAL alone, or their combination prevented TBI-induced the increase of IL-1ß and TNF-α levels, suppressed the up-regulation of ER stress, apoptosis and autophagy after TBI. However, anti-ST2L treatment could significantly invert the above effects of IL-33. Together, these data demonstrate that IL-33/ST2 signaling mitigates TBI-induced brain edema, motor function outcome, spatial learning and memory deficits, at least in part, by a mechanism involving suppressing autophagy, ER stress, apoptosis and neuroinflammation.

[Application of diatom detection using knead pulp method].

OBJECTIVE: A novel technology for detection of diatom was discussed. METHODS: Five grams of testing sample were taken and the organics were removed using simple mechanical knead pulp method. The homogenized samples were concentrated by centrifugation, smeared, and then examined under light microscope. RESULTS: Except for a few feather's grains, the vast majority of diatom could be identified easily with clear diatom striations. The organic diatom could also be easily detected by this methodology. CONCLUSION: The detection of diatom using knead pulp method is not only simple and inexpensive with a higher successful rate, but also causes nearly no harm to human and environment.

The tailored synthesis of nanosized SAPO-34 via time-controlled silicon release enabled by an organosilane precursor.

Phenyltrimethoxysilane as a Si source can significantly slow down the crystallization process for SAPO-34 synthesis, leading to the formation of agglomerated nanocrystals (<100 nm). The obtained nanosized SAPO-34 shows enhanced catalytic stability in methanol-to-olefin conversion under industrially relevant conditions.

IL-33 Provides Neuroprotection through Suppressing Apoptotic, Autophagic and NF-κB-Mediated Inflammatory Pathways in a Rat Model of Recurrent Neonatal Seizure.

Interleukin-33 (IL-33) is a novel identified chromatin-associated cytokine of IL-1 family cytokines. It signals through a heterodimer comprised of ST2L and IL-1RAcp, and plays a crucial role in many diseases. However, very little is known about the role and underlying intricate mechanisms of IL-33 in recurrent neonatal seizure (RNS). To determine whether IL-33 plays an important regulatory role, we established a neonatal seizure model in this study. Rats were subjected to recurrent seizures induced by inhaling volatile flurothyl. Recombinant IL-33 or PBS were also administered by intraperitoneally (IP) before surgery, respectively. Here, our current results indicated that RNS contributed to a significant reduction in IL-33 and its specific receptor (ST2L) expressions in cortex. While, in hippocampus, RNS induced an increase in IL-33 and ST2L evidently, compared with Sham group. After injection with IL-33, however, a remarkable increase in total IL-33 was detected both in brain cortex and hippocampus. In addition, IL-33 was mainly co-localized in the nuclear of GFAP+ astrocytes and the cytoplasm of the Iba-1+ microglia and IL-33+/NeuN+ merged cells. In parallel, ST2L was expressed mainly in the membrane of GFAP+ astrocytes, Iba-1+ microglia and NeuN+ neurons, respectively. Furthermore, administration of IL-33 improved RNS-induced behavioral deficits, promoted bodyweight gain, and ameliorated spatial learning and memory ability. Moreover, IL-33 pretreatment blocked the activation of NF-κB, resisted inflammatory cytokines IL-1ß and TNF-α increase, as well as suppressed apoptosis and autophagy activation after RNS. Collectively, IL-33 provides potential neuroprotection through suppressing apoptosis, autophagy and at least in part by NF-κB-mediated inflammatory pathways after RNS.

Curcumin alleviates brain edema by lowering AQP4 expression levels in a rat model of hypoxia-hypercapnia-induced brain damage.

The present study aimed to investigate the therapeutic effects of curcumin (CU) against brain edema in a rat model of hypoxia-hypercapnia (HH)-induced brain damage (HHBD). Male Sprague-Dawley rats were divided into five groups, including a control group and four treatment groups. The rats in the control group were raised under normal laboratory conditions and were injected with water, whereas the rats in the treatment groups were exposed to a low O2/high CO2 environment simulating HH conditions, and were injected with water, CU, dimethyl sulfoxide (solvent control) or monosialoganglioside GM1. After 2 weeks, the morphological characteristics of the brain tissues were analyzed using optical and electron microscopy. In addition, aquaporin (AQP)-4 protein expression levels in brain tissue samples were analyzed using streptavidin-biotin complex immunohistochemistry and western blotting, and mRNA expression levels were detected using reverse transcription-quantitative polymerase chain reaction. Severe brain edema, tissue structure disruption and increased AQP4 expression levels were detected in the brain tissues of the HH rats. Conversely, the rats treated with CU or GM1 exhibited attenuated HHBD-induced brain edema and tissue structure disruption, and decreased mRNA and protein expression levels of AQP4. The results of the present study suggested that CU treatment was able to attenuate HHBD-induced brain edema by downregulating the expression levels of AQP4 in a rat model. Therefore, CU may be considered a potential therapeutic drug for the treatment of patients with brain edema.

Influences of CCK-8 on expressions of apoptosis-related genes in prefrontal cortex neurons of morphine-relapse rats.

In order to elucidate the influences of CCK-8 on expressions of apoptosis-related genes, Bax, Bcl-2 and Caspase-3, of prefrontal cortex neurons in morphine-relapse rats, an effective, successful morphine-relapse-rat model using the conditioned place preference (CPP) under CCK-8 (0.01, 0.1 and 1.0µg, i.c.v) intervention was established. The prefrontal cortexes were made into slices with the cellular plasmas immunohistochemically stained. The expressions of Bax, Bcl-2, Caspase-3 of neurons were evaluated through their scores, and each corresponding ratio of Bax and Bcl-2 (Bax/Bcl-2) was also computed. The results showed that the expression of Bcl-2 was very weak and those of Bax and Caspase-3 were hardly seen in group normal saline; the expressions of Bax and Caspase-3 were strong and that of Bcl-2 was weak in group morphine and compared to group normal saline, there were significant differences (P<0.05); the expressions of Bax, Caspase-3 and the ratios of Bax/Bcl-2 have a gradually-decreased trend in the sequence of group 0.01µg, group 0.1µg and group 1.0µg, but the expression of Bcl-2 has an opposite trend in the same sequence, and compared to group morphine, there were significant differences (P<0.05) excluding group 0.01µg. So we draw a conclusion that CCK-8 (0.1 and 1.0µg, i.c.v) could protect neurons of prefrontal cortex through up-regulating the expression of Bcl-2, down-regulating those of Bax and Caspase-3 and reducing Bax/Bcl-2 ratio in the model of morphine-relapse rats.

Activation of α7nAChR Promotes Diabetic Wound Healing by Suppressing AGE-Induced TNF-α Production.

Diabetes frequently presents accumulation of advanced glycation end products (AGEs), which might induce excessive TNF-α production from macrophages to cause impaired wound healing. Recent studies have shown that activation of α7 nicotinic acetylcholine receptor (α7nAChR) on macrophages efficiently suppressed TNF-α synthesis. The aim of this study was to investigate the accumulation of AGEs in the wounds and determine whether PNU282987, an α7nAChR agonist, can improve wound repair by inhibiting AGE-mediated TNF-α production in a streptozotocin (STZ)-induced diabetic mouse model. Animals were assigned into four groups: wounded control group, wounded diabetic group, wounded diabetic group treated intraperitoneally with PNU282987, or wounded diabetic group treated intraperitoneally with vehicle. Compared with the non-diabetic control mice, the diabetic mice exhibited delayed wound healing that was characterized by elevated accumulation of AGEs, increased TNF-α level and macrophage infiltration, and decreased fibroblast number and collagen deposition at the late stage of repair. Besides, macrophages of diabetic wounds showed expression of α7nAChR. During late repair, PNU282987 treatment of diabetic mice significantly reduced the level of TNF-α, accelerated wound healing, and elevated fibroblast number and collagen deposition. To investigate the cellular mechanism of these observations, RAW 264.7 cells, a macrophage cell line, were incubated with AGEs in the presence or absence of PNU282987. TNF-α production from AGE-stimulated macrophages was significantly decreased by PNU282987 in a dose-dependent manner. Furthermore, PNU282987 significantly inhibited AGE-induced nuclear factor-κB (NF-κB) activation and receptor for AGE (RAGE) expression. These results strongly suggest that activating α7nAChR can promote diabetic wound healing by suppressing AGE-induced TNF-α production, which may be closely associated with the blockage of NF-κB activation in macrophages.