1.Folic acid treatment regulates C2C12 myoblast diferentiation via JNK/p38 MAPK signaling pathway
Manli SUN ; Haifeng DENG ; Shaoju JIN ; Xudong CHEN ; Xinghong WANG ; Wenjuan FAN
Chinese Journal of Pathophysiology 2024;40(2):317-325
AIM:To observe the effect of folic acid(FA)on C2C12 myoblast proliferation and differentia-tion,and to explore its mechanism.METHODS:During the proliferation stage,C2C12 myoblasts were treated with vari-ous concentrations of FA(0,2.5,5,10 and 20 μmol/L).The cell status was observed under a microscope,cell viability was detected using the MTT method,and cell proliferation was assessed using the EdU method.In the differentiation stage,C2C12 cells were divided into control(Ctrl)group(0 μmol/L FA)and FA group(10 μmol/L FA).On day 2 or 4 of differentiation,immunofluorescence staining and Western blot were employed to detect the expression of myoblast differen-tiation-related proteins,myoblast determination protein 1(MyoD),myogenin(MyoG)and myosin heavy chain(MyHC).The myotubule formation in each group was analyzed.On day 4 of differentiation,C2C12 cells were treated with FA for 0,1,3 and 6 h,and the protein levels of p-JNK,JNK,p-p38 MAPK and p38 MAPK at each time point were detected by Western blot.Additionally,C2C12 cells after 4-day differentiation were divided into Ctrl group,FA group,FA+ SP600125(specific inhibitor of JNK)group,and FA+SB203580(specific inhibitor of p38)group.The cells in FA+ SP600125 and FA+SB203580 groups were treated with 10 μmol/L SP600125 or SB203580 for 1 h,followed by treatment with 10 μmol/L FA for 24 h.The cells in FA group were treated with 10 μmol/L FA for 24 h,while the cells in Ctrl group were left untreated.The protein levels of p-JNK,JNK,p-p38 MAPK,p38 MAPK and MyHC were detected by Western blot.RESULTS:(1)Compared with 0 μmol/L FA group,the number of the cells in other concentration groups in-creased,cell viability was raised(P<0.05 or P<0.01),and the rate of EdU positive cells increased(P<0.05).(2)Com-pared with Ctrl group,the expression levels of MyoD,MyoG and MyHC in FA group were increased(P<0.05),and the myotube fusion index was raised(P<0.05 or P<0.01).(3)Compared with 0 h group,the ratios of p-JNK/JNK and p-p38 MAPK/p38 MAPK were elevated after FA treatment for 1,3 and 6 h(P<0.05 or P<0.01),and showed a trend of gradual increase with the extension of treatment time.(4)After FA treatment,the ratios of p-JNK/JNK and p-p38 MAPK/p38 MAPK,and the expression of MyHC were elevated(P<0.01).Treatment with SP600125 decreased the ratio of p-JNK/JNK and the expression of MyHC(P<0.05),while SB203580 intervention cut down the ratio of p-p38 MAPK/p38 MAPK and the expression of MyHC(P<0.05 or P<0.01).CONCLUSION:Folic acid can promote the differentiation of C2C12 myoblasts by activating the JNK/p38 MAPK signaling pathway.
2.Smoke exposure during adolescence affects learning and memory abili-ties of mice in adulthood via prefrontal microglia-mediated inflammation
Wenjuan FAN ; Yanfeng CHEN ; Zipeng DUAN ; Manli SUN ; Xudong CHEN
Chinese Journal of Pathophysiology 2024;40(12):2254-2261
AIM:To investigate the effects of cigarette smoke exposure during adolescence on the inflammato-ry response mediated by microglia in the prefrontal cortex of mice,and its impact on learning and memory functions in adulthood.METHODS:72 two-week-old healthy male Kunming mice,with each weighing(11.0±1.5)g,were random-ly divided into control and cigarette exposure groups(n=36 per group).The mice in the cigarette exposure group were pas-sively exposed to 6 cigarettes daily for 10 weeks.At three time points of 4-week-old(infancy),8-week-old(adoles-cence),and 12-week-old(adulthood),six mice were selected from each group to have their neurobehavioral and patholog-ical changes examined.In particular,the step-down test,three-chamber social interaction test,and novel object recogni-tion test were used to detect changes in learning and memory abilities and cognitive behavior.Immunofluorescence testing was performed to detect the morphology,number of synapses,and expression of inflammatory factor apoptosis-associated speck-like protein containing a CARD(ASC)around the microglial cells in the prefrontal cortex of mice in each group.Western blot was performed to assess the expression levels of synaptophysin(SYP)and postsynaptic density protein-95(PSD-95)in the cerebral cortex of mice in each group.Enzyme-linked immunosorbent assay(ELISA)was performed to detect the protein expression of tumor necrosis factor-α(TNF-α),interleukin 1β(IL-1β),and IL-6 in the prefrontal cor-tex.RESULTS:(1)In the step-down test,the latency of mice at 8 and 12 weeks of age was significantly shortened,and the number of errors was significantly increased in the cigarette exposure group compared with the age-matched control group(P<0.01).In addition,the social recognition time and exploration time for novel objects were prolonged(P<0.05).(2)Immunofluorescence assays revealed that exposure to cigarette smoke in mice,at both 8 and 12 weeks of age,resulted in a reduction of SYP-positive puncta within the prefrontal cortex.Concurrently,there was an observed increase in the number of Iba1-positive microglia,which exhibited an activated phenotype,as well as an elevation in ASC-positive puncta in proximity to the microglia.Western blot further revealed reduced expression of synaptophysin protein SYP and PSD-95 in the cerebral cortex of the mice at 8 and 12 weeks of age in the cigarette exposure group(P<0.05).(3)ELISA showed increased levels of inflammatory factors TNF-α,IL-1β,and IL-6 in the prefrontal cortex of the mice at 8 and 12 weeks of age in the cigarette exposure group(P<0.05).CONCLUSION:Exposure to cigarette smoke during adoles-cence in mice may result in the enhanced secretion of inflammatory factors through the activation of microglia in the pre-frontal cortex.This activation can alter microglial function and induce synaptic damage,consequently impairing learning,memory,and cognitive abilities in adulthood.
3.Research Progress on the Correlation Between Oral Frailty and Dietary Intake in Older Adults
Manli LIU ; Jingyi WEI ; Wanqing XIE ; Xiaoshuang ZHANG ; Yao WANG ; Mimi WEI ; Fan LIU
Journal of Sichuan University (Medical Sciences) 2024;55(5):1336-1342
With the increase in age,the oral function of older adults shows an age-related decline,which limits the types,quantity,and quality of their diet.Limited dietary intake can lead to a lack of basic nutrients needed for maintaining oral health,induce a series of oral diseases,and further aggravate the deterioration of oral functions.Oral frailty is the accumulation of mild oral function decline and is an emerging concept in the field of oral health.Currently,research on oral frailty and dietary intake mostly focuses on the impact of single-dimensional oral function decline on the dietary intake,dietary structure,and dietary satisfaction of older adults,as well as the impact of different dietary structures on the status of oral health among older adults.There is still a lack of large-sample,high-quality research on the relationship between comprehensive oral function decline and dietary intake.In addition,existing oral frailty intervention measures often place a narrow emphasis on the exercise and recovery of oral function without considering the impact of dietary intake and nutritional status on the development of oral frailty.Relevant research on taking dietary intake as an entry point or using it as a comprehensive intervention method also needs to be further explored by researchers.In the future,specialized assessment and screening of dietary status may be introduced in the routine health management practices for older adults.Furthermore,targeted intervention programs could also be proposed based on the characteristics of the oral status and the dietary intake habits of older adults,so as to prevent the functional decline related to dietary intake and nutritional supplementation.Herein,we reviewed the correlation between dietary intake and oral frailty to provide new ideas and directions for formulating comprehensive management strategies for oral frailty.
4.Smoke exposure during adolescence affects learning and memory abili-ties of mice in adulthood via prefrontal microglia-mediated inflammation
Wenjuan FAN ; Yanfeng CHEN ; Zipeng DUAN ; Manli SUN ; Xudong CHEN
Chinese Journal of Pathophysiology 2024;40(12):2254-2261
AIM:To investigate the effects of cigarette smoke exposure during adolescence on the inflammato-ry response mediated by microglia in the prefrontal cortex of mice,and its impact on learning and memory functions in adulthood.METHODS:72 two-week-old healthy male Kunming mice,with each weighing(11.0±1.5)g,were random-ly divided into control and cigarette exposure groups(n=36 per group).The mice in the cigarette exposure group were pas-sively exposed to 6 cigarettes daily for 10 weeks.At three time points of 4-week-old(infancy),8-week-old(adoles-cence),and 12-week-old(adulthood),six mice were selected from each group to have their neurobehavioral and patholog-ical changes examined.In particular,the step-down test,three-chamber social interaction test,and novel object recogni-tion test were used to detect changes in learning and memory abilities and cognitive behavior.Immunofluorescence testing was performed to detect the morphology,number of synapses,and expression of inflammatory factor apoptosis-associated speck-like protein containing a CARD(ASC)around the microglial cells in the prefrontal cortex of mice in each group.Western blot was performed to assess the expression levels of synaptophysin(SYP)and postsynaptic density protein-95(PSD-95)in the cerebral cortex of mice in each group.Enzyme-linked immunosorbent assay(ELISA)was performed to detect the protein expression of tumor necrosis factor-α(TNF-α),interleukin 1β(IL-1β),and IL-6 in the prefrontal cor-tex.RESULTS:(1)In the step-down test,the latency of mice at 8 and 12 weeks of age was significantly shortened,and the number of errors was significantly increased in the cigarette exposure group compared with the age-matched control group(P<0.01).In addition,the social recognition time and exploration time for novel objects were prolonged(P<0.05).(2)Immunofluorescence assays revealed that exposure to cigarette smoke in mice,at both 8 and 12 weeks of age,resulted in a reduction of SYP-positive puncta within the prefrontal cortex.Concurrently,there was an observed increase in the number of Iba1-positive microglia,which exhibited an activated phenotype,as well as an elevation in ASC-positive puncta in proximity to the microglia.Western blot further revealed reduced expression of synaptophysin protein SYP and PSD-95 in the cerebral cortex of the mice at 8 and 12 weeks of age in the cigarette exposure group(P<0.05).(3)ELISA showed increased levels of inflammatory factors TNF-α,IL-1β,and IL-6 in the prefrontal cortex of the mice at 8 and 12 weeks of age in the cigarette exposure group(P<0.05).CONCLUSION:Exposure to cigarette smoke during adoles-cence in mice may result in the enhanced secretion of inflammatory factors through the activation of microglia in the pre-frontal cortex.This activation can alter microglial function and induce synaptic damage,consequently impairing learning,memory,and cognitive abilities in adulthood.
5.Chinese expert consensus on emergency surgery for severe trauma and infection prevention during corona virus disease 2019 epidemic (version 2023)
Yang LI ; Yuchang WANG ; Haiwen PENG ; Xijie DONG ; Guodong LIU ; Wei WANG ; Hong YAN ; Fan YANG ; Ding LIU ; Huidan JING ; Yu XIE ; Manli TANG ; Xian CHEN ; Wei GAO ; Qingshan GUO ; Zhaohui TANG ; Hao TANG ; Bingling HE ; Qingxiang MAO ; Zhen WANG ; Xiangjun BAI ; Daqing CHEN ; Haiming CHEN ; Min DAO ; Dingyuan DU ; Haoyu FENG ; Ke FENG ; Xiang GAO ; Wubing HE ; Peiyang HU ; Xi HU ; Gang HUANG ; Guangbin HUANG ; Wei JIANG ; Hongxu JIN ; Laifa KONG ; He LI ; Lianxin LI ; Xiangmin LI ; Xinzhi LI ; Yifei LI ; Zilong LI ; Huimin LIU ; Changjian LIU ; Xiaogang MA ; Chunqiu PAN ; Xiaohua PAN ; Lei PENG ; Jifu QU ; Qiangui REN ; Xiguang SANG ; Biao SHAO ; Yin SHEN ; Mingwei SUN ; Fang WANG ; Juan WANG ; Jun WANG ; Wenlou WANG ; Zhihua WANG ; Xu WU ; Renju XIAO ; Yang XIE ; Feng XU ; Xinwen YANG ; Yuetao YANG ; Yongkun YAO ; Changlin YIN ; Yigang YU ; Ke ZHANG ; Xingwen ZHANG ; Guixi ZHANG ; Gang ZHAO ; Xiaogang ZHAO ; Xiaosong ZHU ; Yan′an ZHU ; Changju ZHU ; Zhanfei LI ; Lianyang ZHANG
Chinese Journal of Trauma 2023;39(2):97-106
During coronavirus disease 2019 epidemic, the treatment of severe trauma has been impacted. The Consensus on emergency surgery and infection prevention and control for severe trauma patients with 2019 novel corona virus pneumonia was published online on February 12, 2020, providing a strong guidance for the emergency treatment of severe trauma and the self-protection of medical staffs in the early stage of the epidemic. With the Joint Prevention and Control Mechanism of the State Council renaming "novel coronavirus pneumonia" to "novel coronavirus infection" and the infection being managed with measures against class B infectious diseases since January 8, 2023, the consensus published in 2020 is no longer applicable to the emergency treatment of severe trauma in the new stage of epidemic prevention and control. In this context, led by the Chinese Traumatology Association, Chinese Trauma Surgeon Association, Trauma Medicine Branch of Chinese International Exchange and Promotive Association for Medical and Health Care, and Editorial Board of Chinese Journal of Traumatology, the Chinese expert consensus on emergency surgery for severe trauma and infection prevention during coronavirus disease 2019 epidemic ( version 2023) is formulated to ensure the effectiveness and safety in the treatment of severe trauma in the new stage. Based on the policy of the Joint Prevention and Control Mechanism of the State Council and by using evidence-based medical evidence as well as Delphi expert consultation and voting, 16 recommendations are put forward from the four aspects of the related definitions, infection prevention, preoperative assessment and preparation, emergency operation and postoperative management, hoping to provide a reference for severe trauma care in the new stage of the epidemic prevention and control.
6.Protective effect of Acronychia pedunculata water extract on photoaging keratinocyte model and its mechanism
Xiuling LUO ; Yuan ZHOU ; Binbin ZHAO ; Manli HUANG ; Wenyu LI ; Runge FAN ; Sijian WEN ; Jichao LI ; Huayu WU ; Youkun LIN
Chinese Journal of Medical Aesthetics and Cosmetology 2022;28(6):517-521
Objective:To investigate the protective effect and mechanism of Acronychia pedunculata water extracts on UV-induced light damage of human keratinocytes.Methods:The experiment was conducted from December 2018 to April 2020 in the Guangxi Medical University Laboratory of Genetics. The photoaged keratinocyte model was used, the cells were co-cultured with different concentrations of Acronychia pedunculata water extracts. The cell proliferation rate was detected by CCK-8 method. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and total antioxidant capacity (T-AOC) of cells were detected by a test kit. The levels of IL-1β, IL-6 and tumor necrosis factor-alpha (TNF-α) were determined by ELISA.Results:The proliferation of HaCaT cells was promoted by 0.5 mg/L-2.0 mg/L of the extracts. Compared with control group, the proliferation rate of HaCaT cells in the experimental group was significantly increased ( P<0.05). Compared with control group, the contents of ROS was decreased ( F=214.67, P<0.05), MDA was decreased ( F=811.88, P<0.05), SOD was increased ( F=28.95, P<0.05), CAT was increased ( F=213.31, P<0.05), GPX was increased ( F=65.10, P<0.05), T-AOC was increased ( F=305.58, P<0.05), IL-1β was decreased ( F=15.46, P<0.05), IL-6 was decreased ( F=59.2, P<0.05), and TNF-α was decreased ( F=33.13, P<0.05). Conclusions:The extracts of 0.5-2.0 mg/L of Acronychia pedunculata have protective effects on the photoaging cell model, which may be related to the increase of SOD, CAT, GPX and other antioxidant enzymes and the level of T-AOC in photoaging HaCaT cells, and the decrease of ROS, MDA content and the expression of inflammatory cytokines.
7.Protective effect of vitexin on retinal ganglion cells in rat retinal ischemia-reperfusion injury model
Manli LI ; Ke FAN ; Hongpei CUI
Chinese Journal of Experimental Ophthalmology 2021;39(3):191-197
Objective:To explore the protective effect of vitexin on retinal ganglion stem cells (RGCs) from oxidative stress caused by retinal ischemia-reperfusion (RIR) in rats and its possible mechanism.Methods:Sixty male SD rats were randomly divided into the model group, vitexin group and normal control group by random number table, with 20 rats in each group.The right eyes were taken as experimental eyes.Rats in the model group and the vitexin group were treated with anterior chamber perfusion to establish RIR models.Rats in the vitexin group were given intraperitoneal injection of vitexin at a dose of 25 mg/(kg·d) for 7 days.Rats in the model group were intraperitoneally injected with the same volume of normal saline.For the normal control group, the experimental eyes underwent anterior chamber puncture without increasing the intraocular pressure, and were intraperitoneally injected with the same volume of normal saline.On the 7th day following modeling, the rats were sacrificed by overdose anesthesia.Histopathology staining was used to detect the thickness of retina and the number of RGCs.Retrograde tracing with Fluoro-Gold was used to detect the density of RGCs.TUNEL staining was used to detect the apoptosis of RGCs.Colorimetric method was used to detected superoxidate dismutase (SOD) activity and concentration of malondialdehyde (MDA) and nitric oxide (NO). Western blot method was used to detect the relative expression levels of cytoplasmic Nrf2, HO-1, NQO1, nuclear Nrf2 proteins in rat retina.The use and care of animals followed the ARVO Statement.This study protocol was approved by the Experimental Animal Ethics Committee of Henan Eye Hospital (No.HNEECA-2019-04).Results:The retinal thickness was (90.21±3.55)μm in the model group, which was significantly lower than (128.20±5.31)μm in the normal control group and (119.65±6.14)μm in the vitexin group, and the differences were statistically significant (both at P<0.05). The average density of RGCs was (1 300.85±14.00)/mm 2 in the model group, which was significantly lower than(2 330.12±15.05)/mm 2 in the normal control group and (1 921.64±11.78)/mm 2 in the vitexin group, and the differences were statistically significant (both at P<0.05). The rate of TUNEL positive RGCs was (68.34±5.04)% in the model group, which was significantly higher than (3.01±0.18)% in the normal control group and (35.51±2.04)% in the vitexin group, and the differences were statistically significant (both at P<0.05). Compared with the normal control group and the vitexin group, the SOD activity in the retinal tissue of the rats was lower and the concentrations of MDA and NO were higher in the model group, and the differences were statistically significant (all at P<0.05). The expression level of cytoplasmic Nrf2 protein was the lowest in the vitexin group, then following the model group and the normal control group, and the relative expression levels of HO-1, NQO1 and nuclear Nrf2 protein were the highest in the vitexin group, then followed the model group and normal control group, and the differences were statistically significant (all at P<0.05). Conclusions:Vitexin can reduce the apoptosis of RGCs and alleviate oxidative stress damage of retina in RIR rat model.This protective effect may be achieved by activating Nrf2-related signaling pathway.
8.Submaxillary gland enlargement caused by reduced glutathione
Jingjing YAN ; Yi HAN ; Manli FAN
Adverse Drug Reactions Journal 2021;23(6):319-321
A 44-year-old male patient was hospitalized twice for chronic hepatitis B and alcoholic cirrhosis with hepatic encephalopathy. During the 2 times of hospitalization, the patient was treated with reduced glutathione and ornithine aspartate and developed bilateral submandibular gland enlargement on the 2nd day after the first medication in each hospitalization. Physical examination showed no abnormal skin color and temperature, no obvious tenderness, intact oral mucosa, and no redness and swelling of submandibular gland duct orifice. Ultrasonic examination showed diffuse enlargement of bilateral submandibular gland and visible peripheral lymph nodes and bilateral cervical lymph nodes. It was never aware to be drug-related in the first occurrence of submandibular gland enlargement, therefore the drug was not stopped and no special treatment was given. The patient′s submandibular gland enlargement subsided spontaneously 2 days later. During the 2nd hospitalization, the patient developed bilateral submandibular gland enlargement again, which was considered to be related to reduced glutathione because no submandibular gland enlargement appeared in the patient during the repeated use of ornithine aspartate in the past. Then the reduced glutathione was stopped and ornithine aspartate was continued. The patient′s submandibular gland enlargement subsided completely 1 day later.
9.Submaxillary gland enlargement caused by reduced glutathione
Jingjing YAN ; Yi HAN ; Manli FAN
Adverse Drug Reactions Journal 2021;23(6):319-321
A 44-year-old male patient was hospitalized twice for chronic hepatitis B and alcoholic cirrhosis with hepatic encephalopathy. During the 2 times of hospitalization, the patient was treated with reduced glutathione and ornithine aspartate and developed bilateral submandibular gland enlargement on the 2nd day after the first medication in each hospitalization. Physical examination showed no abnormal skin color and temperature, no obvious tenderness, intact oral mucosa, and no redness and swelling of submandibular gland duct orifice. Ultrasonic examination showed diffuse enlargement of bilateral submandibular gland and visible peripheral lymph nodes and bilateral cervical lymph nodes. It was never aware to be drug-related in the first occurrence of submandibular gland enlargement, therefore the drug was not stopped and no special treatment was given. The patient′s submandibular gland enlargement subsided spontaneously 2 days later. During the 2nd hospitalization, the patient developed bilateral submandibular gland enlargement again, which was considered to be related to reduced glutathione because no submandibular gland enlargement appeared in the patient during the repeated use of ornithine aspartate in the past. Then the reduced glutathione was stopped and ornithine aspartate was continued. The patient′s submandibular gland enlargement subsided completely 1 day later.
10.Investigation of medical social work in Chinese hospitals.
Zhe CHEN ; Zhicheng GONG ; Xujie HAO ; Manli WANG ; Xuegong FAN
Journal of Central South University(Medical Sciences) 2019;44(7):818-822
To understand the development of medical social work in China, and provide reference and basis for promoting medical social work in the next stage.
Methods: A random sampling method was used to survey and analyze the data from questionnaires distributed to hospitals at or above the second level in China.
Results: Medical social work had been carried out in all parts of the country, but the development was not balanced with the establishment of specialized agencies accounting for about 7.9% of the total survey. Only 17.5% of the hospitals carried out medical social work as a routine work. The medical social work service mainly included volunteer operation and management, patient psychological counseling, and so on.
Conclusion: The development of medical social work in hospitals in China is still in its infancy, and the regional development is not balanced. Lack of professionals, unclear responsibilities of medical social workers and low social identity of medical social work are the main factors restricting development.
Asian Continental Ancestry Group
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China
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Hospitals
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Humans
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Social Work
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Surveys and Questionnaires

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