ObjectiveTo observe the effects of Yangjing Zhongyutang （YJZYT） on mitochondrial biogenesis and oxidative stress damage mediated by the silent information regulator 1 （SIRT1）/peroxisome proliferator-activated receptor gamma coactivator-1alpha （PGC-1α） signaling pathway in cyclophosphamide （CTX）-induced rats with diminished ovarian reserve （DOR）， and to explore its mechanism in improving ovarian reserve function and follicular development. MethodsForty-two 8-week-old female SD rats with normal estrous cycles were randomly divided into a blank control group （n=7） and a model group （n=35）. Rats in the model group received a single intraperitoneal injection of CTX （90 mg·kg^-1） to establish the DOR model. After modeling， estrous cycles were monitored for 7 consecutive days， and model success was confirmed based on criteria for estrous cycle disruption. After successful modeling， rats were divided into groups for intervention： estradiol valerate group （0.09 mg·kg^-1）， and YJZYT high-， medium-， and low-dose groups （19.98， 9.99， 5.00 g·kg^-1）. The blank control group and model group were given an equal volume of distilled water by gavage. All groups received daily gavage once for 4 consecutive weeks. The general state， body weight， and ovarian wet weight of rats were observed and recorded， and the ovarian organ index was calculated. Enzyme-linked immunosorbent assay （ELISA） was used to measure serum levels of follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， estradiol （E₂）， anti-Müllerian hormone （AMH）， superoxide dismutase （SOD）， and glutathione peroxidase （GSH-Px）. Hematoxylin-eosin （HE） staining was performed to observe ovarian histomorphological changes and follicular development status. Immunofluorescence was used to detect reactive oxygen species （ROS） expression levels. Colorimetric assays were employed to measure adenosine triphosphate （ATP） and malondialdehyde （MDA） content in ovarian tissues. Quantitative Real-time polymerase chain reaction （Real-time PCR） was used to detect mitochondrial DNA （mtDNA） copy number and the mRNA expression levels of key genes including SIRT1， PGC-1α， nuclear respiratory factor 1 （NRF1）， and mitochondrial transcription factor A （TFAM）. Western blot was performed to detect the protein expression levels of SIRT1， PGC-1α， NRF1， and TFAM. ResultsCompared with the blank group， rats in the model group exhibited disrupted estrous cycles， obviously reduced body weight， and decreased ovarian index （P<0.05）. Ovarian histopathology revealed cortical thinning， loose structure， and a significant reduction in both primordial and growing follicles （P<0.01）. Serum FSH and LH levels were significantly elevated （P<0.01）， while E₂ and AMH levels were obviously reduced （P<0.05， P<0.01）. ATP content and mtDNA copy number decreased in ovarian tissue （P<0.01）， ROS expression increased， MDA levels rose， while SOD and GSH-Px activities obviously decreased （P<0.05， P<0.01）， mRNA and protein expression levels of SIRT1， PGC-1α， NRF1， and TFAM were obviously downregulated （P<0.05， P<0.01）. After treatment， compared with the model group， body weight and ovarian index obviously recovered in rats administered various doses of YJZYT （P<0.05）， serum E₂ and AMH levels increased， while FSH and LH levels obviously decreased （P<0.05， P<0.01）， ovarian tissue ATP content and mtDNA copy number were up-regulated， ROS and MDA levels decreased， and antioxidant enzymes SOD and GSH-Px activity obviously increased （P<0.05， P<0.01）， Gene and protein expression levels related to the SIRT1/PGC-1α /NRF1/TFAM signaling pathway were obviously up-regulated compared to the model group （P<0.05， P<0.01）， HE staining revealed that ovarian structure gradually recovered to integrity in all treatment groups， with a obviously increase in the number of primordial and growing follicles （P<0.05， P<0.01）. Granulosa cells were neatly arranged， indicating marked improvement in ovarian function. ConclusionYJZYT may improve ovarian function and follicular development in rats with diminished ovarian reserve by activating the SIRT1/PGC-1α signaling pathway， promoting mitochondrial biogenesis， enhancing mitochondrial function， and alleviating oxidative stress damage.

OBJECTIVE: To review recent advances in the application of hair transplantation in wound healing and scar repair in special areas. METHODS: An extensive review of the literature on the application of hair transplantation in wound healing and scar repair in special areas was conducted, focusing on cellular functions, molecular mechanisms, and clinical applications. RESULTS: Hair transplantation has been shown to effectively promote wound healing and scar repair in special areas. The underlying mechanisms are complex, but current understanding emphasizes a strong association with hair follicle-associated stem cells (including epidermal stem cells, dermal papilla cells, dermal sheath cells, etc). CONCLUSION The application of hair transplantation in wound healing and scar repair in special areas remains in its early stages. Further investigation into its mechanisms of action is essential, and randomized controlled trials are needed to establish its efficacy.
Humans ; Wound Healing/physiology* ; Cicatrix/therapy* ; Hair/transplantation* ; Hair Follicle/transplantation*

Objective To predict and analyze the"properties-efficacy"of foreign medicinal resource Moringa oleifera leaves by taking"Xiang"based on plant phylogenetic relationships and component structural characteristics.Methods The properties of Moringa oleifera were determined by screening plants with its genetic relationship.Network pharmacology was used to study the biological network characteristics of Moringa oleifera leaves and related Chinese materia medica,and the"properties-efficacy"of Moringa oleifera leaves was studied based on the"xiang"of medicinal plants.Using"the relationship chart between the efficacy of Chinese materia medica and 12 types of chemical components",the possible efficacy and distribution of medicinal properties of Moringa oleifera leaves were predicted,and a study on the"properties-efficacy"characteristics of Moringa oleifera leaves was conducted based on the structural features of the components.Results Moringaceae and Caricaceae had a genetic relationship in plant classification;Moringa oleifera leaves,Carica papaya and Carica papaya leaves had a relatively high number of common targets,common clinical phenotypes and signaling pathways.The large proportion of coincidence showed that Moringa oleifera leaves might have similar functional performance and mechanism to Carica papaya and Carica papaya leaves;Moringa oleifera leaves contain flavonoids,tannins,monophenols,which were related to the efficacy of Chinese materia medica on tonifying qi,dispersing wind heat,cooling blood and regulating qi.Clustering analysis method was used to get the corresponding"properties-efficacy"relationship,and the results indicated that Moringa oleifera leaves were cool in property and sweet in taste,which belonged to lung meridian and had the efficacy of dispersing wind heat.Conclusion It is feasible to predict and analyze the"properties-efficacy"of foreign medicinal resources by taking"xiang".

Objective:To summarize the experience of repairing partial areolar necrosis following reduction mammaplasty.Methods:A retrospective analysis was conducted on clinical data from patients who experienced partial areola necrosis after reduction mammaplasty. These patients were treated or consulted at the Department of Plastic Surgery, Zhongshan Hospital, Fudan University, between January 2017 and February 2023. Preoperatively, daily dressing changes were performed on the necrotic areola wounds until the boundaries of necrosis were clearly defined. Debridement and repair were then carried out by resecting bilateral breast glandular tissue through the original incision to reduce breast volume, followed by narrowing the areola radius. If no areola defect remained after narrowing, direct suturing was performed; if defects persisted, the resected normal areola skin was used for grafting. Postoperative follow-up was conducted to observe areola recovery and complications. At the 6-month postoperative mark, patient satisfaction was evaluated using a 5-level scale (very satisfied, satisfied, neutral, dissatisfied, very dissatisfied). An experienced plastic physician, not involved in the surgery, assessed areolar outcomes based on four criteria: color, softness, shape, and scarring, with each criterion scored from 1 to 4 (higher scores indicating better outcomes).Results:Eight female patients (9 necrotic areolas) were included in the study, with a mean age of (31.8±5.4) years and a mean body mass index of (24.1±1.8) kg/m 2. Among the 9 necrotic areolas, 3 had defect areas greater than 50% of the total areola area, while 6 had defects less than 50%. Direct suturing after areola narrowing was performed in 3 areolas, while free areola skin grafting was used in 6 areolas. Postoperatively, 2 cases exhibited mild epidermal erosion at the graft site, which improved with dressing changes. No complications such as infection, bleeding, hematoma, or seroma occurred. At the 6-month follow-up, all 8 patients demonstrated good wound healing, and all 9 areolas survived. The areolas exhibited consistent shape and color bilaterally, without significant pigmentation changes, depigmentation, or irregular shapes. In the 6 grafted areolas, the grafted skin color closely matched the surrounding native areola tissue, with no obvious demarcation or scar hyperplasia. Patient satisfaction was rated as very satisfied in 3 cases and satisfied in 5 cases. According to the physician’s evaluation, the scores for color, softness, shape, and scarring were (3.7±0.5), (3.8±0.4), (3.3±0.7) and (3.2±0.7) points, respectively. Conclusion:Partial areola necrosis following reduction mammaplasty can be effectively repaired by further reducing breast volume and narrowing the areola for direct suturing or by grafting excess areola skin to the defect site. A satisfactory appearance can be achieved after surgery.

Aim To investigate the effect of hydrogen sulfide on macrophage calcification and its underlying mo-lecular mechanisms.Methods Oil red O staining was used to observe intracellular lipid accumulation,and von Kossa staining and atomic absorption spectroscopy were used for morphological and quantitative analysis of calcium deposition and intracellular calcium content in a mononuclear macrophage calcification model.Western blot and RT-PCR were used to detect the mRNA and protein expression of osteopontin(OPN)at different doses and treatment times of hydrogen sulfide.At the same time,Western blot was used to detect the expression changes of early growth response factor 1(EGR1),endo-plasmic reticulum stress-related markers C/EBP homologous protein(CHOP)and glucose-regulated protein 78(GRP78).Reactive oxygen species levels were evaluated by fluorescence probe staining,and the effect of hydrogen sulfide on macro-phage calcification was evaluated by combining von Kossa staining and calcium ion fluorescence probe staining.The mo-lecular mechanisms of hydrogen sulfide affecting macrophage calcification were explored by interfering with EGR1 expression and using endoplasmic reticulum stress inhibitor 4-phenylbutyric acid(4-PBA).Results Compared with oxidized low density lipoprotein(ox-LDL)group,β-glycerophosphate(β-GP)+40 g/L ox-LDL group showed a significant increase in intracellular lipid accumulation,while hydrogen sulfide significantly inhibited macrophage calcification in a con-centration-and time-dependent manner.Compared with the β-GP+ox LDL group,the most significant effect was observed after incubation with 100 μmol/L NaHS for 4 days.The hydrogen sulfide group showed a 66％decrease in intracellular calcium content(P＜0.01),a 71％decrease in intercellular calcium deposition(P＜0.01),and a 50％and 48％decrease in OPN mRNA and protein expression,respectively(P＜0.05).Hydrogen sulfide treatment upregulated the ex-pression of EGR1 by 21％,while downregulating the expression of CHOP and GRP78 by 58％and 59％,respectively(P＜0.01).The endoplasmic reticulum stress inhibitor 4-PBA could downregulate OPN expression by 73％(P＜0.01),while interfering with EGR1 expression completely counteracts the inhibitory effect of hydrogen sulfide on OPN expression and calcium deposition(P＜0.01).Conclusion Hydrogen sulfide significantly inhibits macrophage calcification by upregulating EGR1 expression and suppressing endoplasmic reticulum stress.

Objective:Nailfold video capillaroscopy (NVC) was used to evaluate the microvascular changes in patients with connective tissue diseases (CTD)-related Raynaud′s phenomenon and explore its potential application value in understanding the pathogenesis, diagnosis, and treatment of CTD.Methods:The literature on NVC of connective tissue disease related patients published by CNKI, China biomedical literature database, Weipu Database,Wanfang Database, PubMed, Embase, Web of Science and Cochrane were searched, and the publication cases of time was up until May 2024. Quality assessment of the included studies was performed using the National Institutes of Health observational cohort and cross-sectional study quality assessment tools. Begg′s test and Egger′s test were analyzed with random effects meta-analysis.Results:A total of 12 studies were included, including 495 cases of Raynaud′s phenomenon of Connective tissue diseases, and 716 no-Raynaud′s phenomenon of Connective tissue diseases. The abnormal rate of nail microcirculation in CTDs-RP group was higher than that in CTDs-nonRP group [ OR value(95% CI)=2.20 (1.55, 3.12), P<0.001], Subgroup analysis showed that the proportion of scleroderma pattern in the CTDs-RP group was higher than that in the control group [ OR value (95% CI)=10.88 (2.34, 50.52), P=0.002], Telangiectasia rate in the CTDs-RP group was higher than that in the control group [ OR value (95% CI)=5.12 (3.40, 7.70), P<0.001]. The SSc pattern was higher in patients with CTD-RP than in the control group [ OR (95% CI)=2.47 (1.60, 3.79), P<0.001], The rate of capillary malformation in the CTD-RP group was higher than that in the control group [ OR value (95% CI)=2.39 (1.36, 4.19), P=0.002], The capillary density was mild decreased in the CTD-RP group [SMD value (95% CI)=-0.27 (-0.66, 0.13), P=0.185]. Conclusion:The proportion of patients with nail-fold abnormality is higher in CTD-RP group was higher than in the CTD-noRP group, and the microcirculation injury is more severe in CTD-RP group.

Objective:To evaluate the effect of arctigenin (ARG) on cognitive dysfunction induced by sevoflurane anesthesia in aged rats and the role of autophagy-mediated pyroptosis.Methods:Fifty SPF male Sprague-Dawley rats, aged 18-20 months, weighing 550-600 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (C group), sevoflurane anesthesia group (Sev group), sevoflurane anesthesia+ ARG group (Sev+ ARG group), sevoflurane anesthesia+ autophagy inducer rapamycin group (Sev+ RAPA group), and sevoflurane anesthesia+ ARG+ autophagy inhibitor 3-methyladenine (3-MA) group (Sev+ ARG+ 3-MA group). Except for group C, the rats in the other groups inhaled 6% sevoflurane for 3 h to establish the cognitive impairment model. At 30 min before anesthesia, ARG 20 mg/kg was intraperitoneally injected in Sev+ ARG group, rapamycin 7.5 mg/kg was intraperitoneally injected in Sev+ RAPA group, and ARG 20 mg/kg (dissolved in dimethyl sulfoxide) was intraperitoneally injected, followed by immediate intraperitoneal injection of 3-MA 1.5 mg/kg in Sev+ ARG+ 3-MA group. The equal volume of dimethyl sulfoxide was intraperitoneally injected in C group and Sev group. The Morris water maze test was conducted to assess the cognitive function at 48 h after the end of administration. After completion of the Morris water maze test, the hippocampal tissue was taken under deep anesthesia for observation of the pathological changes (after HE staining) which were scored and for determination of neuronal pyroptosis (after propidium iodide staining) and expression of neuronal autophagy-related proteins (microtubule-associated protein 1 light chain 3 [LC3], Beclin-1, p62), pyroptosis-related proteins (NOD-like receptor protein 3 [NLRP3], apoptosis-associated speck-like protein containing a CARD [ASC], pro-cysteine aspartate-specific protease 1 [pro-caspase-1], cleaved-caspase-1, gasdermin D [GSDMD], and N-terminal fragment of gasdermin D [GSDMD-N], interleukin-1β [IL-1β] and IL-18). Results:Compared with C group, the escape latency was significantly prolonged, the time of staying at the original platform quadrant was shortened, the number of crossing the original platform was reduced, the hippocampal injury score and neuronal pyroptosis rate were increased, LC3Ⅱ/LC3Ⅰ ratio was decreased, the expression of Beclin-1 was down-regulated, the expression of p62, NLRP3, ASC, IL-1β and IL-18 was up-regulated, and the cleaved-caspase-1/pro-caspase-1 ratio and GSDMD-N/GSDMD ratio were increased in Sev group ( P<0.05). Compared with Sev group, the escape latency was significantly shortened, the time of staying at the original platform quadrant was prolonged, the number of crossing the original platform was increased, the hippocampal injury score and neuronal pyroptosis rate were decreased, LC3Ⅱ/LC3Ⅰ ratio was increased, the expression of Beclin-1 was up-regulated, the expression of p62, NLRP3, ASC, IL-1β and IL-18 was down-regulated, and the cleaved-caspase-1/pro-caspase-1 ratio and GSDMD-N/GSDMD ratio were decreased in Sev+ ARG group and Sev+ RAPA group ( P<0.05). Compared with Sev+ ARG group, the escape latency was significantly prolonged, the time of staying at the original platform quadrant was shortened, the number of crossing the original platform was reduced, the hippocampal injury score and neuronal pyroptosis rate were increased, LC3Ⅱ/LC3Ⅰ ratio was decreased, the expression of Beclin-1 was down-regulated, the expression of p62, NLRP3, ASC, IL-1β and IL-18 was up-regulated, and the cleaved-caspase-1/pro-caspase-1 ratio and GSDMD-N/GSDMD ratio were increased in Sev+ ARG+ 3-MA group ( P<0.05). Conclusions:AGR can alleviate sevoflurane anesthesia-induced cognitive dysfunction in aged rats, and the mechanism is related to reduction of autophagy-mediated cell pyroptosis.

Objective:To evaluate the effect of arctigenin (ARG) on cognitive dysfunction induced by sevoflurane anesthesia in aged rats and the role of autophagy-mediated pyroptosis.Methods:Fifty SPF male Sprague-Dawley rats, aged 18-20 months, weighing 550-600 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (C group), sevoflurane anesthesia group (Sev group), sevoflurane anesthesia+ ARG group (Sev+ ARG group), sevoflurane anesthesia+ autophagy inducer rapamycin group (Sev+ RAPA group), and sevoflurane anesthesia+ ARG+ autophagy inhibitor 3-methyladenine (3-MA) group (Sev+ ARG+ 3-MA group). Except for group C, the rats in the other groups inhaled 6% sevoflurane for 3 h to establish the cognitive impairment model. At 30 min before anesthesia, ARG 20 mg/kg was intraperitoneally injected in Sev+ ARG group, rapamycin 7.5 mg/kg was intraperitoneally injected in Sev+ RAPA group, and ARG 20 mg/kg (dissolved in dimethyl sulfoxide) was intraperitoneally injected, followed by immediate intraperitoneal injection of 3-MA 1.5 mg/kg in Sev+ ARG+ 3-MA group. The equal volume of dimethyl sulfoxide was intraperitoneally injected in C group and Sev group. The Morris water maze test was conducted to assess the cognitive function at 48 h after the end of administration. After completion of the Morris water maze test, the hippocampal tissue was taken under deep anesthesia for observation of the pathological changes (after HE staining) which were scored and for determination of neuronal pyroptosis (after propidium iodide staining) and expression of neuronal autophagy-related proteins (microtubule-associated protein 1 light chain 3 [LC3], Beclin-1, p62), pyroptosis-related proteins (NOD-like receptor protein 3 [NLRP3], apoptosis-associated speck-like protein containing a CARD [ASC], pro-cysteine aspartate-specific protease 1 [pro-caspase-1], cleaved-caspase-1, gasdermin D [GSDMD], and N-terminal fragment of gasdermin D [GSDMD-N], interleukin-1β [IL-1β] and IL-18). Results:Compared with C group, the escape latency was significantly prolonged, the time of staying at the original platform quadrant was shortened, the number of crossing the original platform was reduced, the hippocampal injury score and neuronal pyroptosis rate were increased, LC3Ⅱ/LC3Ⅰ ratio was decreased, the expression of Beclin-1 was down-regulated, the expression of p62, NLRP3, ASC, IL-1β and IL-18 was up-regulated, and the cleaved-caspase-1/pro-caspase-1 ratio and GSDMD-N/GSDMD ratio were increased in Sev group ( P<0.05). Compared with Sev group, the escape latency was significantly shortened, the time of staying at the original platform quadrant was prolonged, the number of crossing the original platform was increased, the hippocampal injury score and neuronal pyroptosis rate were decreased, LC3Ⅱ/LC3Ⅰ ratio was increased, the expression of Beclin-1 was up-regulated, the expression of p62, NLRP3, ASC, IL-1β and IL-18 was down-regulated, and the cleaved-caspase-1/pro-caspase-1 ratio and GSDMD-N/GSDMD ratio were decreased in Sev+ ARG group and Sev+ RAPA group ( P<0.05). Compared with Sev+ ARG group, the escape latency was significantly prolonged, the time of staying at the original platform quadrant was shortened, the number of crossing the original platform was reduced, the hippocampal injury score and neuronal pyroptosis rate were increased, LC3Ⅱ/LC3Ⅰ ratio was decreased, the expression of Beclin-1 was down-regulated, the expression of p62, NLRP3, ASC, IL-1β and IL-18 was up-regulated, and the cleaved-caspase-1/pro-caspase-1 ratio and GSDMD-N/GSDMD ratio were increased in Sev+ ARG+ 3-MA group ( P<0.05). Conclusions:AGR can alleviate sevoflurane anesthesia-induced cognitive dysfunction in aged rats, and the mechanism is related to reduction of autophagy-mediated cell pyroptosis.

Aim To investigate the effect of hydrogen sulfide on macrophage calcification and its underlying mo-lecular mechanisms.Methods Oil red O staining was used to observe intracellular lipid accumulation,and von Kossa staining and atomic absorption spectroscopy were used for morphological and quantitative analysis of calcium deposition and intracellular calcium content in a mononuclear macrophage calcification model.Western blot and RT-PCR were used to detect the mRNA and protein expression of osteopontin(OPN)at different doses and treatment times of hydrogen sulfide.At the same time,Western blot was used to detect the expression changes of early growth response factor 1(EGR1),endo-plasmic reticulum stress-related markers C/EBP homologous protein(CHOP)and glucose-regulated protein 78(GRP78).Reactive oxygen species levels were evaluated by fluorescence probe staining,and the effect of hydrogen sulfide on macro-phage calcification was evaluated by combining von Kossa staining and calcium ion fluorescence probe staining.The mo-lecular mechanisms of hydrogen sulfide affecting macrophage calcification were explored by interfering with EGR1 expression and using endoplasmic reticulum stress inhibitor 4-phenylbutyric acid(4-PBA).Results Compared with oxidized low density lipoprotein(ox-LDL)group,β-glycerophosphate(β-GP)+40 g/L ox-LDL group showed a significant increase in intracellular lipid accumulation,while hydrogen sulfide significantly inhibited macrophage calcification in a con-centration-and time-dependent manner.Compared with the β-GP+ox LDL group,the most significant effect was observed after incubation with 100 μmol/L NaHS for 4 days.The hydrogen sulfide group showed a 66％decrease in intracellular calcium content(P＜0.01),a 71％decrease in intercellular calcium deposition(P＜0.01),and a 50％and 48％decrease in OPN mRNA and protein expression,respectively(P＜0.05).Hydrogen sulfide treatment upregulated the ex-pression of EGR1 by 21％,while downregulating the expression of CHOP and GRP78 by 58％and 59％,respectively(P＜0.01).The endoplasmic reticulum stress inhibitor 4-PBA could downregulate OPN expression by 73％(P＜0.01),while interfering with EGR1 expression completely counteracts the inhibitory effect of hydrogen sulfide on OPN expression and calcium deposition(P＜0.01).Conclusion Hydrogen sulfide significantly inhibits macrophage calcification by upregulating EGR1 expression and suppressing endoplasmic reticulum stress.