Ferroptosis is a unique regulated form of cell death that is distinct from apoptosis, necrosis, and other well-characterized regulated cell death types, and plays an important role in the occurrence and development of chronic metabolic diseases, including diabetes, hypertension, hyperlipidemia, and non-alcoholic steatohepatitis. Recently, increasing evidence has supported traditional Chinese medicine (TCM) as a new hot spot for the treatment of chronic metabolic diseases by mediating ferroptosis. Unfortunately, few systematic reviews have described the importance of TCM in treating chronic metabolic diseases through the ferroptosis pathway. In the current review, the mechanism of ferroptosis and the roles of ferroptosis in chronic metabolic diseases are summarized. Additionally, this review illustrates that the regulation of ferroptosis by TCM could be an effective approach for treating chronic metabolic diseases based on experimental evidence and clinical application. In summary, this work will improve the understanding of ferroptosis and the ability of TCM to regulate ferroptosis in chronic metabolic diseases, thereby promoting the development and application of natural TCM.

OBJECTIVE To study the protective effect and mechanism of Bupleurum chinense polysaccharides （BCP） on acute liver injury （ALI） in mice. METHODS Overall 40 mice were randomly divided into normal group， model group， positive control group （Baogan tablet， 550 mg/kg）， BCP high-dose and low-dose groups （400， 100 mg/kg）， with 8 mice in each group. The drug was administered intragastrical once a day for 7 days. One hour after the last administration， except for the normal group， mice in other groups were injected with 20 mg/kg concanavalin A solution through the tail vein to establish ALI model. After injection of concanavalin A solution for 12 h， the liver and spleen indexes of mice were measured， and the pathological changes of liver and spleen tissue were observed； the serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT） and lactate dehydrogenase （LDH） were detected， and the levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in liver tissue were detected. The levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6） and IL-1β in serum and liver tissue of mice were determined， as well as the protein expression levels of nuclear factor-κB （NF-κB）， Toll-like receptor 4 （TLR4）， nuclear factor erythroid 2-related factor 2 （Nrf2） and heme oxygenase-1 （HO-1） in liver tissue were also detected. RESULTS Compared with the normal group， the liver tissue of mice in the model group was necrotic and infiltrated with inflammatory cells； spleen enlargement， increased bleeding and decreased lymphocytes were observed， liver and spleen indexes were increased significantly （P＜0.01）； the serum levels of AST， ALT and LDH， the levels of TNF-α， IL-6 and IL-1β in serum and liver tissue， as well as the MDA level， protein expressions of TLR4， NF- κB and HO-1 in liver tissue were all increased significantly （P＜0.05 or P＜0.01）. The levels of SOD and protein expression of Nrf2 in liver tissue were all decreased significantly （P＜0.05）. Compared with the model group， the pathological damages of the liver and the spleen tissues in mice alleviated in BCP high-dose and low-dose groups， and most of liver and spleen indexes， the above indexes of serum and liver tissue were reversed significantly （P＜0.05 or P＜0.01）. CONCLUSIONS BCP has a protective effect on ALI， the mechanism of which may be related to the inhibition of TLR4/NF-κB signaling pathway and the activation of the Nrf2/HO-1 signaling pathway.

Objective:To investigate the mechanism of trigger point deactivation induced by pressing manipulation in a rat model and to explore its potential regulation of the inflammatory response through the extracellular signal-regulated kinase(ERK)/nuclear factor-κB(NF-κB)pathway. Methods:Fifty male Sprague-Dawley rats were randomly divided into a blank group,a model group,a pressing manipulation group,an ERK agonist group,and a pressing manipulation+ERK agonist group,with 10 rats in each group.Except for the blank group,rats in other groups were used to establish the trigger point rat model using the blunt blow combined with the eccentric exercise method.The pressing manipulation group underwent pressing manipulation intervention at the trigger points.The ERK agonist group received an injection of recombinant human epidermal growth factor via the tail vein.The pressing manipulation+ERK agonist group received interventions from both the pressing manipulation and ERK agonist groups.The pressure pain threshold(PPT)was measured by a mechanical pain threshold detector before and after the intervention.The histological changes were evaluated by hematoxylin-eosin staining after the intervention;the expression levels of ERK,phosphorylated ERK(p-ERK),NF-κB p65(p65),phosphorylated NF-κB p65(p-p65),and phosphorylated NF-κB inhibitor(p-IκB)were detected by Western blotting;the levels of interleukin(IL)-1β,IL-6,and tumor necrosis factor(TNF)-α were detected by enzyme-linked immunosorbent assay. Results:The PPT increased(P<0.05);the inflammatory cells disappeared;the ratios of p-ERK/ERK,p-p65/p65,and p-IκB/β-actin,also the levels of IL-1β,IL-6,and TNF-α all decreased in the pressing manipulation group after the intervention compared with the model group(P<0.05).The PPT decreased significantly(P<0.05),the inflammatory cell presence increased,and the ratios of p-ERK/ERK and p-p65/p65 were elevated(P<0.05);additionally,the levels of IL-6 and TNF-α were significantly higher in the pressing manipulation+ERK agonist group compared with the pressing manipulation group(P<0.05).The PPT was significantly lower(P<0.05),the inflammatory cell count was higher,the ratios of p-ERK/ERK and p-IκB/β-actin and the levels of IL-1β and TNF-α were significantly higher in the ERK agonist group compared with the pressing manipulation+ERK agonist group(P<0.05). Conclusion:Pressing manipulation can effectively alleviate inflammation and pain in trigger point model rats,potentially by inhibiting the ERK/NF-κB signaling pathway.

Traditional Chinese medicine has the characteristics of multiple components， pathways， and targets in the treatment of fracture healing， and has good therapeutic advantages and potential for fractures with complex pathological mechanisms. Based on this， the author summarized the mechanism of promoting fracture healing by the monomer components and compound formulas of traditional Chinese medicine and found that visfatin A， puerarin， and others can activate the mitogen-activated protein kinase （MAPK） signaling pathway； Xugudan， Guben zenggu formula and others can activate bone morphogenetic protein （BMP） signaling pathway； baicalin， Achyranthes bidentata polysaccharides and others can activate Wnt/β -catenin signaling pathway； apigenin， notoginsenoside and others can activate receptor activator of nuclear factor-κB （NF-κB）/receptor activator of NF-κB ligand/osteoprotegerin （RANK/RANKL/OPG） signaling pathway； Compound huoxue jiegu capsule， Jiangu granule and others can inhibit phosphoinositide 3-kinase/protein kinase B （PI3K/AKT） signaling pathway； icariin can activate Notch signaling pathway； Taohong siwu decoction， crocin and others can activate Hippo signaling pathway； jujuboside A and osthole can inhibit NF-κB signaling pathway， and thus promote fracture healing.

Epilepsy is a chronic brain disease characterized by seizures， and is one of the most common nervous system diseases in clinic practice with the recurrent， transient， and refractory characteristics. Clinically， western medicine therapy is mainly adopted in the treatment of epilepsy， but it is not conducive to long-term use for patients on account of severe side effects， which can result in abnormalities in the digestive system， central nervous system， hematopoietic system， urinary system， and liver function to varying degrees. Syndrome differentiation is usually used for the treatment of epilepsy by traditional Chinese medicine （TCM）， which can avoid the side effects of western medicine treatment on the basis of improving patients' syndromes. The literature on TCM in the treatment of epilepsy in China and abroad indicates that the syndrome differentiation in TCM is often based on phlegm， blood stasis， wind， and deficiency， and the treatment methods include acupuncture， acupoint catgut embedding， moxibustion， Chinese medicine monomer， drug pair， and compound decoction. The various treatments of TCM play an important role in the comprehensive treatment of epilepsy through multiple channels and links， such as reducing the degree and number of seizures. This paper comprehensively summarized the clinical experience of TCM in the treatment of epilepsy， systematically expounded various treatment methods and ideas of TCM in the treatment of epilepsy， and deeply discussed the mechanism of TCM in the treatment of epilepsy， aiming to provide a theoretical basis for the clinical formulation of a reasonable individualized treatment plan for epilepsy and diversified ideas for the more effective treatment of epilepsy by TCM.

Objective: To explore the mechanism of An-Pressing manipulation in relieving energy crisis in chronic myofascial trigger points (MTrPs) by observing the effects of An-Pressing manipulation on adenosine triphosphate (ATP), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) pathway and mitochondrial ultrastructure of skeletal muscle cells in MTrPs rats. Methods: Forty-eight male Sprague-Dawley rats were randomly divided into a blank group, a model group, a lidocaine group, and an An-Pressing manipulation group, with 12 rats in each group. The model group, lidocaine group and An-Pressing manipulation group were used to replicate the MTrPs rat model by blunt shock and centrifugal motion method. After modeling, the An-Pressing manipulation group was subjected to 7 times An-Pressing manipulation, once every other day; the lidocaine group was treated with 3 times of injection of lidocaine at the MTrPs, once every 6 d. The blank group and the model group were fed normally without intervention. After the intervention, local muscle tissue was taken to detect the content of ATP and the expression of AMPK, phosphorylated AMPK (phospho-AMPK), PGC-1α, and glucose transporter 4 (GluT4), and the ultrastructure of mitochondria was observed under an electron microscope. Results: Compared with the blank group, the ATP content in the model group was decreased (P<0.05), the protein expression levels of phospho-AMPK, PGC-1α, and GluT4 and the ratio of phospho-AMPK to AMPK were decreased (P<0.05); under the electron microscope, the number of mitochondria decreased, and they were deformed, small in volume, and had deformed cristae. Compared with the model group, the ATP contents in the An-Pressing manipulation group and the lidocaine group were increased (P<0.05), and the protein expression levels of phospho-AMPK, PGC-1α, and GluT4 and the ratio of phospho-AMPK to AMPK were increased (P<0.05); under the electron microscope, the number of mitochondria increased, the shape and size of the mitochondria were basically normal, and the cristae could be seen. Compared with the lidocaine group, phospho-AMPK and the ratio of phospho-AMPK to AMPK in the An-Pressing manipulation group were increased (P<0.05); under the electron microscope, the numbers of mitochondria were similar, and the shape and size of the mitochondria were basically normal without swelling, and the cristae could be observed. Conclusion: An-Pressing manipulation can increase the ATP content in MTrPs tissue, improve the expression levels of PGC-1α and GluT4 proteins and the ratio of phospho-AMPK to AMPK; its mechanism may relate to the activation of AMPK/PGC-1α signaling pathway to promote the repair of mitochondrial damages.

Worldwide, gastric cancer is the second leading cause of cancer deaths and the fifth most common malignant tumor. Gastric cancer is believed to be caused by a variety of factors, such as genetics, epigenetics, and environmental influences. Among the pathogenic factors, inflammation has been considered as one of the main risk factors for gastric cancer. There are currently limited ways to prevent gastric cancer. Although the combined application of aspirin and non-steroidal anti-inflammatory drugs can reduce the risk, it has great side effects and can easily cause gastric perforation or gastric bleeding. Therefore, an alternative plan is urgently needed. Curcumin is the yellow pigment in the rhizome of the plant turmeric. Current studies have found that curcumin has a protective effect on gastric mucosal damage caused by non-steroidal anti-inflammatory drugs, gastric mucosal damage in rats, and gastric mucosal damage caused by stress bleeding and Helicobacter pylori infection. Curcumin shows significant anti-inflammatory and anti-cancer activities by regulating DNA methylation, histone modification, nuclear factor erythrocyte 2 related factor 2 and other related signal pathways. In this article, the latest evidence of curcumin for epigenetic changes in gastric cancer and its potential contribution to gastric cancer were discussed.

Poor ovarian response (POR) is usually defined as low ovarian reserve and poor ovarian response to exogenous gonadotropins. The Bologna criteria proposed by the European Society of Human Reproduction and Embryology (ESHRE) in 2011 reached the initial consensus on the diagnostic criteria for POR, but the heterogeneity of these patients has posed many difficulties and doubts on treatment. The POSEIDON criteria, proposed in 2016, allow for stratification based on the heterogeneous features of POR patients and the accurate definition of clinical characteristics and diagnostic criteria for each stratum, leading to precise treatment and improved clinical outcomes for POR patients. This article reviews the background of the latest POSEIDON criteria, the characteristics of the stratified population and the progress of corresponding treatment studies.

Poor ovarian response (POR) is usually defined as low ovarian reserve and poor ovarian response to exogenous gonadotropins. The Bologna criteria proposed by the European Society of Human Reproduction and Embryology (ESHRE) in 2011 reached the initial consensus on the diagnostic criteria for POR, but the heterogeneity of these patients has posed many difficulties and doubts on treatment. The POSEIDON criteria, proposed in 2016, allow for stratification based on the heterogeneous features of POR patients and the accurate definition of clinical characteristics and diagnostic criteria for each stratum, leading to precise treatment and improved clinical outcomes for POR patients. This article reviews the background of the latest POSEIDON criteria, the characteristics of the stratified population and the progress of corresponding treatment studies.

Objective:To investigate the effect of low dosage of human chorionic gonadotropin (hCG) replacing human menopausal gonadotropin (hMG) in the late follicular stage during progestin-primed ovarian stimulation (PPOS) on the outcome of in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI) for polycystic ovary syndrome (PCOS) patients. Methods:The patients with PCOS who underwent IVF/ICSI-frozen-thawed embryo transfer (FET) treatment in the Department of Assisted Reproduction of Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine from March 2015 to December 2017 were retrospectively analyzed. Ovarian stimulation adopted PPOS. According to whether low dosage of hCG was used to replace hMG in the late follicular stage of PPOS, they were divided into two groups: group A, PPOS routine group (hMG + progesterone), complete application of hMG (141 cycles); group B, hMG/hCG+progesterone, low dosage of hCG (200 IU/d) was used to completely replace hMG in the late follicular stage of PPOS (80 cycles). The clinical data and pregnancy related indexes of the two groups were compared. The main outcome measures included the number of oocytes retrieved, the number of available embryos and clinical pregnancy rate.Results:There was no significant difference in the duration of ovarian stimulation between group A and group B [(9.7±2.6) d vs. (10.3±3.4) d, P=0.16]. The duration of hMG administration [(7.8±3.5) d] and the dosage of hMG [(1 592.8±840.5) IU] in group B were significantly lower than those in group A [(9.7±2.6) d, P=0.01; (1 825.2±795.3) IU, P=0.04]. There were no significant differences in the number of oocytes retrieved (17.3±8.9 vs.17.8±8.8) and the number of available embryos (6.2±4.1 vs. 6.0±3.2) between the two groups ( P>0.05). In the subsequent FET cycle, the clinical pregnancy rate [52.8% (105/199) vs. 49.2% (60/122)], the embryo implantation rate [37.1% (139/375) vs. 37.1% (86/232)], the early abortion rate [4.8% (5/105) vs. 5.0% (3/60)] and the ongoing pregnancy rate [47.7% (95/199) vs. 44.3% (54/122)] were not statistically different between group A and group B. Conclusion:The use of low dosage of hCG instead of hMG in the late follicular stage of PPOS in patients with PCOS, which can safely and effectively maintain follicular growth and development, without affecting the outcome of IVF/ICSI-FET for PCOS patients.