Jing Jiang's research while affiliated with Beijing University of Chinese Medicine and Pharmacology and other places

Background: Alzheimer’s disease may be effectively treated with acupoint-based acupuncture, which is acknowledged globally. However, more research is needed to understand the alterations in acupoints that occur throughout the illness and acupuncture treatment. Objective: This research investigated the differences in acupoint microcirculation between normal mice and AD animals in vivo. This research also examined how acupuncture affected AD animal models and acupoint microcirculation. Methods: 6-month-old SAMP8 mice were divided into two groups: the AD group and the acupuncture group. Additionally, SAMR1 mice of the same month were included as the normal group. The study involved subjecting a group of mice to 28 consecutive days of acupuncture at the ST36 (Zusanli) and CV12 (Zhongwan) acupoints. Following this treatment, the Morris water maze test was conducted to assess the mice’s learning and memory abilities; the acoustic-resolution photoacoustic microscope (AR-PAM) imaging system was utilized to observe the microcirculation in CV12 acupoint region and head-specific region of each group of mice. Results: In comparison to the control group, the mice in the AD group exhibited a considerable decline in their learning and memory capabilities (p < 0.01). In comparison to the control group, the vascular in the CV12 region and head-specific region in mice from the AD group exhibited a considerable reduction in length, distance, and diameter r (p < 0.01). The implementation of acupuncture treatment had the potential to enhance the aforementioned condition to a certain degree. Conclusions: These findings offered tangible visual evidence that supports the ongoing investigation into the underlying mechanisms of acupuncture’s therapeutic effects.

As stimulation points in acupuncture,acupoints have unique local pathological characteristics. Acupoint sensitization is the transformation of an acupoint from a ‘silent state’ to an‘activ ated state’ and the specificity of sensitization is important for disease investigation, and its dynamics vary significantly with the degree of sensitization.The mechanism of action of l ocal acupoints on the skin needs to be further clarified to provide reference value for sub sequent acupuncture treatment.To explore the degree of acupoint sensitization relatedto the and the underlying mechanism of local content of small biomolecules, mainly mastcells.We established a knee osteoarthritis (KOA) model by intra-articular injection of sodiumiodoac etate (MIA) into the left knee of rats.The distal points of the extremities (Left Tianjing,Ri ght Tianjing,Left Heding,Right Heding)were selected for the study.The mechanical pain thre shold at local acupoints was detected by Electric Von Frey, and the aggregation andthreshi ng status of mast cells(MCs) were detected by toluidine blue staining.The MCs aggregatio n and degranulation status of each group were detected by toluidine blue staining;the chan ges in the content of trypsin, 5-HT and HA indexes at different activation points weredete cted by immunofluorescence double-labeling method.It showed that the content of trypsin, 5-HT and HA at different activated acupuncture points varied more than the resting state of the local acupuncture points, with the right Tianjing acupoint having a higher content t han the other points, indicating that the number of MCs and the content of trypsin, 5-HT and HA produced by degranulation may be one of the cellular mechanisms occurring dur ing acupuncture point sensitization. The pain thresholds of different acupoints were signific antly different, and the sensitization degree was in the order of right Tianjing acupoint（SJ 10）>right Heding acupoint（EX-LE2）>left Heding acupoint（EX-LE2）>left Tianjing acu point（SJ10）.It indicated that the sensitization differences clarify the degrees of variationw ith the differences in point selection,which helped to broaden the understanding ofthe char acteristics of local points and explore the basic pathology of localpoints and provided som e theoretical basis for clinical intervention selection.

Objective: The goal was to investigate the connection between neuroinflammation in the brain and serum inflammatory markers as Alzheimer's disease progressed. We also sought to determine whether electroacupuncture had an effect on inflammatory markers found in blood and other brain regions. Methods: As an animal model for AD, we used senescence-accelerated mouse prone 8 (SAMP8) mice. To examine the effects and probable mechanism of electroacupuncture, we used HE staining, immunofluorescence staining, western blotting, and enzyme-linked immunosorbent assay. Results: Electroacupuncture therapy protected neurons, significantly downregulated the Iba-1 level in the hippocampus (p value was 0.003), frontal lobe cortex (p value was 0.042), and temporal lobe cortex (p value was 0.013) of the AD animal model, all of which had significantly lower levels of IL-6 (p value was 0.001), IL-1β (p value was 0.001), and TNF-α (p value was 0.001) in their serum. Conclusion: The amounts of IL-6, IL-1β, and TNF-α detected in the serum were strongly linked to the levels discovered in the hippocampus and the frontal lobes of the brain, respectively. A better understanding of the electroacupuncture process as well as the course of Alzheimer's disease and the therapeutic benefits of electroacupuncture may be gained by using biomarkers such as serum inflammatory marker biomarkers.

Objective To explore the mechanism by which electroacupuncture (EA) upregulates triggering receptor expressed on myeloid cells 2 (TREM2) protein in the hippocampus of Alzheimer’s disease (AD) model animals from the perspective of TREM2 DNA methylation. Methods In total, 24 eight-month-old senescence-accelerated mouse prone 8 (SAMP8) mice were divided into an (untreated) AD group (n = 8), donepezil group (receiving donepezil treatment, n = 8) or EA group (receiving an EA intervention, n = 8). A healthy control group comprising 8-month-old senescence-accelerated mouse resistant 1 (SAMR1) mice (n = 8) was also included. Western blotting, bisulfite sequencing, and oxidative bisulfite sequencing were applied to test the relative expression of TREM2 protein and the methylation levels of the TREM2 gene. Results EA significantly upregulated the relative expression of TREM2 protein (p < 0.01), downregulated the 5-methylcytosine level (p < 0.01) and upregulated the 5-hydroxymethylcytosine level (p < 0.05) in the hippocampus. Conclusion Downregulation of 5-methylcytosine levels and upregulation of 5-hydroxymethylcytosine levels in the TREM2 gene might be the mechanism by which EA promotes the expression of TREM2 protein.

Alzheimer's disease (AD), as one of most common dementia, mainly affects older people from the worldwide. In this study, we intended to explore the possible mechanism of improving cognitive function and protecting the neuron effect by electroacupuncture. Method: We applied senescence-accelerated mouse prone 8 (SAMP8) mice as AD animal model, used Morris water maze, HE staining, 16S rDNA amplicon sequencing of gut microbiota and ELISA to demonstrate our hypothesis. Results: electroacupuncture improved the learning and memory abilities in SAMP8 mice (P<0.05) and could protect the frontal lobe cortex and hippocampus of SAMP8 mice; electroacupuncture significantly decreased the expression of IL-1β (P<0.01), IL-6 (P<0.01) and TNF-α (P<0.01 in hippocampus, P<0.05 in serum) in serum and hippocampus; electroacupuncture balanced the quantity and composition of gut microbiome, especially of the relative abundance in Delta-proteobacteria (P<0.05) and Epsilon-proteobacteria (P<0.05). Conclusion: electroacupuncture treatment could inhibit the peripheral and central nerve system inflammatory response by balancing the gut microbiota.

Objective: To observe the changes of microvascular structure of acupoints caused by myocardial ischemia, so as to explore the application of photoacoustic imaging technology in the research of acupoint sensitization. Methods: Twelve BALB/c mice were randomly divided into normal, sham operation and acute myocardial ischemia (AMI) model groups, with 4 mice in each group. AMI model was established by ligating the left anterior descending coronary artery. Electrocardiogram (ECG) was recorded by physiological signal acquisition system at 12 h and on the 14th day after modeling, and serum cardiac troponin T (cTnT) and creatine kinase isoenzyme MB (CK-MB) levels were detected by enzyme-linked immunosorbent assay. The microvascular structure changes of acupoints "Feishu"(BL13), "Jueyinshu"(BL14), "Quze"(PC3) and "Chize"(LU5) were observed by photoacoustic imaging technology, and distance (DM), inflection count metric (ICM), sum of angle metric(SOAM)and microvessel density (MVD) were calculated by microvascular quantification algorithm. Results: Compared with the normal and sham operation groups, the ST segment of ECG was obviously elevated, serum cTnT and CK-MB were significantly increased in AMI model group at 12 h and on the 14th day after AMI (P<0.01). The ICM of BL14 in AMI model group was significantly decreased on the 14th day than that on the 7th day after AMI. Compared with the normal group, the ICM of BL14 was significantly increased in AMI model group on the 7th day after AMI(P<0.05). There were no significant changes in DM, ICM, SOAM and MVD at other acupoints on the 7th and 14th day (P>0.05) among the three groups. Conclusion: The change of ICM may be one of the characteristics of acupoint sensitization and photoacoustic imaging technology can be used to study the structure of acupoint microvessels.

Objective: To explore the effect of electroacupuncture (EA) on the ability of spatial learning-memory and the expression of IL-1β, IL-6 and TNF-α in the hippocampus and spleen tissues and the number of hippocampal neurons and spleen lymphocytes in Alzheimer's disease (AD) mice, so as to study its mechanisms underlying improvement of AD. Methods: Twenty-four SAMP8 mice were randomly and equally divided into AD model, EA and medication groups, and 8 SAMR1 mice were used as the control group. EA (2 Hz, 0.1 mA) was applied to "Baihui"(GV20) and "Yintang"(EX-HN3) for 20 min in the EA group, and intragastric administration of donepezil hydrochloride (0.92 mg/kg) was applied in the medication group, once daily for 15 d. The learning-memory ability was determined by Morris water maze task, and the histopathological changes of hippocampus were observed after H.E. staining, followed by determining neurons and the number of splenic lymphocytes. The expression levels of IL-1β, IL-6 and TNF-α in the hippocampus and spleen were detected by immunohistochemistry and Western blot, respectively. Results: After mode-ling, the escape latency of place navigation test in the Morris water maze, the spleen index, immunoactivity and expression levels of IL-1β, IL-6 and TNF-α proteins in the hippocampus and spleen tissues were significantly increased (P<0.05, P<0.01). Compared with the model group, the escape latency, spleen index, immunoactivity and expression levels of IL-1β, IL-6 and TNF-α proteins in both hippocampus and spleen were significantly down-regulated in the medication (except the escape latency) and EA groups (P<0.01, P<0.05). The effect of EA was evidently superior to that of medication in shortening the escape latency, lowering the spleen index, and immunoactivity of hippocampal IL-6 and splenic TNF-α immunoactivity (P<0.01, P<0.05). Outcomes of H.E. staining showed disordered arrangement of neurons with nuclear pyknosis or apoptosis in partial neurons in the hippocampus, and thickened and swollen spleen capsule tissue with loose structure and an increased number of lymphocytes in the model group, which was relatively milder in the EA and medication groups. Conclusion: EA can improve the learning-memory ability of AD mice, which may be associated with its effect in relieving the inflammation reaction in the hippocampus and spleen tissues.

Alzheimer's disease (AD) is one of the most serious public health concerns facing the world. Its characteristic feature is neuroinflammation due to microglial activation. Electroacupuncture is one of the therapies employed to improve the condition of patients with AD, although its mechanism of action is still to be determined. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglia-specific receptor that is involved in regulating neuroinflammation in AD. In this study, we applied senescence-accelerated mouse-prone 8 mice as the AD animal model, used the Morris water maze, and applied hematoxylin and eosin staining, immunofluorescence double staining, and Western blotting, to explore the effects and potential mechanisms of action of electroacupuncture. In summary, this study suggested that electroacupuncture treatment could improve the learning and memory abilities (p<0.05) and protect neurons. These effects result from acupuncture could upregulate TREM2 expression in the hippocampus (p<0.01), which was essential for the anti-inflammatory effects in the AD animal model. However, further studies are needed to conclusively demonstrate the mechanism of action of electroacupuncture in AD.

Background The astrocytic phospholipase A2 (PLA2)-arachidonic acid (AA) pathway is crucial in understanding the reduction of cerebral blood flow (CBF) prior to cognitive deterioration. In complementary and alternative medicine, manual acupuncture (MA) is used as one of the most important therapies for Alzheimer’s disease (AD). The beneficial effects of MA on CBF were reported in our previous study. However, the underlying molecular mechanism remains largely elusive. Objective To investigate the effect of MA on the astrocytic PLA2-AA pathway in SAMP8 mice hippocampi. Methods SAMP8 mice were divided into the SAMP8 control (Pc) group, the SAMP8 MA (Pm) group and the SAMP8 donepezil (Pd) group. SAMR1 mice were used as the SAMRl control (Rc) group. Mice in the Pd group were treated with donepezil hydrochloride at 0.65 μg/g. In the Pm group, MA was applied at Baihui (GV20) and Yintang (GV29) for 20 min. The above treatments were administered once a day for 26 consecutive days. The Morris water maze was applied to assess spatial learning and memory. Immunofluorescence staining, western blot and liquid chromatography-tandem mass spectrometry were used to investigate the expression of related proteins and measure the contents of the metabolic intermediates of the PLA2-AA pathway. Results Compared with that in the Rc group, the escape latency in the Pc group significantly increased (p < 0.01); whereas, the platform crossover number and percentage of time and swimming distance in the platform quadrant decreased (p < 0.01). The hippocampal expression of PLA2, cyclooxygenase-1, cytochrome P450 proteins 2C23 and the levels of AA, prostaglandin E2 and epoxyeicosatrienoic acids of the Pc group was drastically higher than that in the Rc group (p < 0.01). These changes were reversed by MA and donepezil (p < 0.01 or p < 0.05). Conclusion MA can effectively improve the learning and memory abilities of SAMP8 mice and has a negative regulatory effect on the PLA2-AA pathway. We propose that the increase of the arterial tone, which is induced by the inhibition of vasodilatory pathway, may be a reason for the beneficial effect of MA on CBF.