BACKGROUND:Activation of nuclear factor-κB/NOD-like receptor thermal protein domain associated protein 3(NLRP3)signaling leads to endothelial dysfunction,oxidative stress,and plays a key role in the initiation of lipid metabolism disorders and arteriosclerosis.However,currenty,the effect of walnut oil and peanut oil on skeletal muscle inflammatory factors in arteriosclerotic rats remains unclear.OBJECTIVE:To discuss the effect and mechanism of walnut oil and peanut oil on atherosclerosis.METHODS:Forty 8-week-old SD male rats were randomly divided into normal control group(n=10)and high fat group(n=30)after 1 week of adaptive feeding.The atherosclerosis model was established by high-fat diet combined with vitamin D3 injection.The rats with successful modeling were randomly divided into model group(n=10),peanut oil group(n=8)and walnut oil group(n=8).The latter two groups were gavaged with peanut oil or walnut oil for 4 weeks(5 days/week,1.2 g/kg per day).After the intervention,ELISA was used to detect the related indexes of blood lipids in rats.The morphological changes of aorta were observed by hematoxylin-eosin staining.The RT-qPCR and western blot assay were used to detect nuclear factor-κB,NLRP3,Caspase-1,interleukin-1β,interleukin-18 mRNA and nuclear factor-κB,NLRP3,interleukin-1β protein expression levels in skeletal muscle.The protein expressions of nuclear factor-κB and NLRP3 were detected by immunofluorescence immunohistochemical staining.RESULTS AND CONCLUSION:(1)Compared with the normal control group,the aortic wall of rats in the model group was thickened,the damage and lipid precipitation were more serious,the blood lipid levels and arteriosclerosis index were significantly increased(P＜0.01).The mRNA levels of nuclear factor-κB,NLRP3,Caspase-1,interleukin-1β,and interleukin-18,and the protein expressions of nuclear factor-κB,NLRP3,and interleukin-1β in skeletal muscle were significantly increased(P＜0.01).(2)Compared with model group,the vulnerable area of aortic tissue in peanut oil group and walnut oil group was significantly reduced,the levels of total cholesterol,triglyceride,low density lipoprotein cholesterol in serum,and atherosclerosis index were decreased(P＜0.01),and the mRNA expressions of nuclear factor-κB,NLRP3,Caspase-1,interleukin-1β,and interleukin-18 and the protein expressions of nuclear factor-κB,NLRP3,and interleukin-1β in skeletal muscle were significantly decreased(P＜0.01 or P＜0.05).(3)Compared with peanut oil group,the serum total cholesterol,triglyceride,and low density lipoprotein cholesterol levels in walnut oil group were significantly decreased(P＜0.01 or P＜0.05),and the mRNA levels of nuclear factor-κB,NLRP3,Caspase-1,interleukin-18,and the protein levels of nuclear factor-κB,NLRP3,interleukin-1β decreased significantly in skeletal muscle(P＜0.01 or P＜0.05).It is concluded that both peanut oil and walnut oil have ameliorative effect on atherosclerotic damage,which may be related to nuclear factor-κB/NLRP3 signaling pathway,and walnut oil has better ameliorative effect than peanut oil.

Rhinovirus (RV) has been reported as one of the main viral causes of human respiratory infections and has received increasing attention in recent years due to its strong association with various respiratory diseases. Studies have shown that RV not only causes the common cold but also plays a critical role in lower respiratory tract conditions such as bronchiolitis, pneumonia, and asthma. Notably, RV is implicated in both the onset and exacerbation of asthma. This review systematically summarizes a wide range of RV-associated respiratory diseases in the available literature. Although there are currently no specific antiviral therapies or vaccines targeting RV, advances in the development of polyvalent vaccines and antiviral drugs provide promising directions for future prevention and treatment. Clarifying the relationship between RV and diseases will provide strong support for optimizing treatment strategies and preventing and controlling respiratory diseases.

BACKGROUND:Exercise interventions play a key role in disease prevention and treatment,which can effectively activate the nuclear factor erythroid2-related factor 2(Nrf2)signaling pathway to prevent the occurrence and development of insulin resistance.However,the potential mechanism of Nrf2-targeting exercise therapy strategies in alleviating insulin resistance remains unclear.OBJECTIVE:Based on the relationship between Nrf2,insulin resistance and exercise,to analyze the mechanism and influence of different exercise modes on the activation of Nrf2,thereby elucidating the potential mechanism of Nrf2-targeting exercise therapy strategies in the process of alleviating insulin resistance.METHODS:"Diabetes mellitus,insulin,insulin resistance,nuclear factor E2 related factor 2,oxidative stress,ferroptosis,autophagy,inflammatory response,exercise"were used as search terms in Chinese and English.WanFang Database,CNKI,Google Scholar and PubMed database were searched for relevant literature from inception to October 2024,and a total of 127 core related articles were obtained according to the inclusion and exclusion criteria.RESULTS AND CONCLUSION:(1)Keap1/Nrf2 signaling pathway,as an important endogenous antioxidant stress pathway,plays an important role in insulin resistance.Activation of Keap1/Nrf2 signaling pathway can enhance the antioxidant capacity of cells,reduce oxidative stress and inflammation,improve insulin signaling,and thus protect insulin resistance.(2)A variety of exercise methods(including aerobic exercise,resistance exercise and high-intensity intermittent exercise)can effectively activate Nrf2 signal,improve the activity of antioxidant kinase and enhance the antioxidant capacity of cells,so as to alleviate oxidative stress damage to a certain extent.(3)By activating Nrf2 signaling pathway,exercise can up-regulate the activity of antioxidant enzymes such as Heme oxygenase 1,superoxide dismutase,catalase,glutathione peroxidase,glutathione,and enhance the antioxidant capacity of cells.In addition,it can also regulate the key enzymes and proteins in the ferroptosis pathway,such as glutathione peroxidase 4,membrane iron transport protein 1,and ferritin heavy chain 1,inhibit the ferroptosis pathway and promote the balance of iron metabolism.In autophagy,the expression of autophagy related genes p62 and ATG5/7 can be enhanced,and the level of microtubule-associated protein 1 light chain 3 is increased,thus regulating autophagy process.At the same time,the activity of tumor necrosis factor-α,nuclear factor-κB,interleukin-6,interleukin-1β and other pro-inflammatory cytokines is decreased,and the inflammatory response can be effectively inhibited.These combined effects can reduce oxidative stress damage,increase insulin sensitivity and improve insulin signaling,and thus have a positive effect on improving insulin resistance.(4)Given that the Keap1/Nrf2 signaling pathway plays an important role in the pathogenesis and treatment of insulin resistance,exercise therapy strategies targeting the Keap1/Nrf2 signaling pathway will help promote the development of"exercise+drug"precision medicine for insulin resistance.

BACKGROUND:Exercise interventions play a key role in disease prevention and treatment,which can effectively activate the nuclear factor erythroid2-related factor 2(Nrf2)signaling pathway to prevent the occurrence and development of insulin resistance.However,the potential mechanism of Nrf2-targeting exercise therapy strategies in alleviating insulin resistance remains unclear.OBJECTIVE:Based on the relationship between Nrf2,insulin resistance and exercise,to analyze the mechanism and influence of different exercise modes on the activation of Nrf2,thereby elucidating the potential mechanism of Nrf2-targeting exercise therapy strategies in the process of alleviating insulin resistance.METHODS:"Diabetes mellitus,insulin,insulin resistance,nuclear factor E2 related factor 2,oxidative stress,ferroptosis,autophagy,inflammatory response,exercise"were used as search terms in Chinese and English.WanFang Database,CNKI,Google Scholar and PubMed database were searched for relevant literature from inception to October 2024,and a total of 127 core related articles were obtained according to the inclusion and exclusion criteria.RESULTS AND CONCLUSION:(1)Keap1/Nrf2 signaling pathway,as an important endogenous antioxidant stress pathway,plays an important role in insulin resistance.Activation of Keap1/Nrf2 signaling pathway can enhance the antioxidant capacity of cells,reduce oxidative stress and inflammation,improve insulin signaling,and thus protect insulin resistance.(2)A variety of exercise methods(including aerobic exercise,resistance exercise and high-intensity intermittent exercise)can effectively activate Nrf2 signal,improve the activity of antioxidant kinase and enhance the antioxidant capacity of cells,so as to alleviate oxidative stress damage to a certain extent.(3)By activating Nrf2 signaling pathway,exercise can up-regulate the activity of antioxidant enzymes such as Heme oxygenase 1,superoxide dismutase,catalase,glutathione peroxidase,glutathione,and enhance the antioxidant capacity of cells.In addition,it can also regulate the key enzymes and proteins in the ferroptosis pathway,such as glutathione peroxidase 4,membrane iron transport protein 1,and ferritin heavy chain 1,inhibit the ferroptosis pathway and promote the balance of iron metabolism.In autophagy,the expression of autophagy related genes p62 and ATG5/7 can be enhanced,and the level of microtubule-associated protein 1 light chain 3 is increased,thus regulating autophagy process.At the same time,the activity of tumor necrosis factor-α,nuclear factor-κB,interleukin-6,interleukin-1β and other pro-inflammatory cytokines is decreased,and the inflammatory response can be effectively inhibited.These combined effects can reduce oxidative stress damage,increase insulin sensitivity and improve insulin signaling,and thus have a positive effect on improving insulin resistance.(4)Given that the Keap1/Nrf2 signaling pathway plays an important role in the pathogenesis and treatment of insulin resistance,exercise therapy strategies targeting the Keap1/Nrf2 signaling pathway will help promote the development of"exercise+drug"precision medicine for insulin resistance.

BACKGROUND:Activation of nuclear factor-κB/NOD-like receptor thermal protein domain associated protein 3(NLRP3)signaling leads to endothelial dysfunction,oxidative stress,and plays a key role in the initiation of lipid metabolism disorders and arteriosclerosis.However,currenty,the effect of walnut oil and peanut oil on skeletal muscle inflammatory factors in arteriosclerotic rats remains unclear.OBJECTIVE:To discuss the effect and mechanism of walnut oil and peanut oil on atherosclerosis.METHODS:Forty 8-week-old SD male rats were randomly divided into normal control group(n=10)and high fat group(n=30)after 1 week of adaptive feeding.The atherosclerosis model was established by high-fat diet combined with vitamin D3 injection.The rats with successful modeling were randomly divided into model group(n=10),peanut oil group(n=8)and walnut oil group(n=8).The latter two groups were gavaged with peanut oil or walnut oil for 4 weeks(5 days/week,1.2 g/kg per day).After the intervention,ELISA was used to detect the related indexes of blood lipids in rats.The morphological changes of aorta were observed by hematoxylin-eosin staining.The RT-qPCR and western blot assay were used to detect nuclear factor-κB,NLRP3,Caspase-1,interleukin-1β,interleukin-18 mRNA and nuclear factor-κB,NLRP3,interleukin-1β protein expression levels in skeletal muscle.The protein expressions of nuclear factor-κB and NLRP3 were detected by immunofluorescence immunohistochemical staining.RESULTS AND CONCLUSION:(1)Compared with the normal control group,the aortic wall of rats in the model group was thickened,the damage and lipid precipitation were more serious,the blood lipid levels and arteriosclerosis index were significantly increased(P＜0.01).The mRNA levels of nuclear factor-κB,NLRP3,Caspase-1,interleukin-1β,and interleukin-18,and the protein expressions of nuclear factor-κB,NLRP3,and interleukin-1β in skeletal muscle were significantly increased(P＜0.01).(2)Compared with model group,the vulnerable area of aortic tissue in peanut oil group and walnut oil group was significantly reduced,the levels of total cholesterol,triglyceride,low density lipoprotein cholesterol in serum,and atherosclerosis index were decreased(P＜0.01),and the mRNA expressions of nuclear factor-κB,NLRP3,Caspase-1,interleukin-1β,and interleukin-18 and the protein expressions of nuclear factor-κB,NLRP3,and interleukin-1β in skeletal muscle were significantly decreased(P＜0.01 or P＜0.05).(3)Compared with peanut oil group,the serum total cholesterol,triglyceride,and low density lipoprotein cholesterol levels in walnut oil group were significantly decreased(P＜0.01 or P＜0.05),and the mRNA levels of nuclear factor-κB,NLRP3,Caspase-1,interleukin-18,and the protein levels of nuclear factor-κB,NLRP3,interleukin-1β decreased significantly in skeletal muscle(P＜0.01 or P＜0.05).It is concluded that both peanut oil and walnut oil have ameliorative effect on atherosclerotic damage,which may be related to nuclear factor-κB/NLRP3 signaling pathway,and walnut oil has better ameliorative effect than peanut oil.

Rhinovirus (RV) has been reported as one of the main viral causes of human respiratory infections and has received increasing attention in recent years due to its strong association with various respiratory diseases. Studies have shown that RV not only causes the common cold but also plays a critical role in lower respiratory tract conditions such as bronchiolitis, pneumonia, and asthma. Notably, RV is implicated in both the onset and exacerbation of asthma. This review systematically summarizes a wide range of RV-associated respiratory diseases in the available literature. Although there are currently no specific antiviral therapies or vaccines targeting RV, advances in the development of polyvalent vaccines and antiviral drugs provide promising directions for future prevention and treatment. Clarifying the relationship between RV and diseases will provide strong support for optimizing treatment strategies and preventing and controlling respiratory diseases.

The neurofilament proteins (NFPs) from different neuronal tissues including Alzheimer and Huntington disease gray matter, rat brain gray, white matter and spinal cord were separated biochemically into two major fractions. A systematic investigation on the distribution, expression and phosphorylation of NFPs in those fractions was undertaken in the present study. It was found that only non-phosphorylated NF-H and NF-M, but not NF-L subunit were detected in Alzheimer brain gray matter high speed supernatant, whereas all neurofilament subunits including non-phosphorylated and phosphorylated were measured in high speed pellet fraction of the same tissue. The hyperphosphorylation of NF-H and NF-M in Alzheimer brain was shown by phosphorylation dependent monoclonal antibodies SMI31 and SMI34. This hyperphosphorylation was confirmed by non-phosphorylation dependent antibody SMI32 with dephosphosphorylation of the samples. Furthermore, an increased amount of NF-H, NH-M and NF-L, detected by SMI33 and NR4 respectively, was also observed in Alzheimer samples, in which the elevation in NF-L was significant. A significantly different immunoblot patterns in distribution, expression and phosphorylation were determined in various position of the neural system and alternative fractions. To our best knowledge, this is the first data shown definite abnormality of NFPs in Alzheimer disease. The information obtained in the present study will be extremely valuable in further study of the proteins both in physiological and pathological conditions.

Objective To investigate the relationship between protein phosphatase inhibition, tau hyperphosphorylation and neuronal death seen in Alzheimer disease (AD). Methods Co culture of protein phosphatase inhibitor okadaic acid (OA) and neuroblastoma cells (SH SY5Y), by agarose gel electrophoresis to detect DNA fragmentation, and in situ hybridization by TdT mediated biotin labeled dNTP nick end labeling (TUNEL) to further detect the cell apoptosis. Results Incubation of SY5Y cells with 10 nmol/L OA for 24 or 48 hours led to the appearance of DNA fragmentation and a remarkable increase of positive cells from 2 16%?0 94% to 18 05%?3 57% ( P