BACKGROUND:Flap transplantation technique is a commonly used surgical procedure for the treatment of severe tissue defects,but postoperative flap necrosis is easily triggered by ischemia-reperfusion injury.Therefore,it is still an important research topic to improve the survival rate of transplanted flaps. OBJECTIVE:To review the pathogenesis and latest treatment progress of flap ischemia-reperfusion injury. METHODS:CNKI,WanFang Database and PubMed database were searched for relevant literature published from 2014 to 2024.The search terms used were"flap,ischemia-reperfusion injury,inflammatory response,oxidative stress,Ca2+overload,apoptosis,mesenchymal stem cells,platelet-rich plasma,signaling pathways,shock wave,pretreatment"in Chinese and English.After elimination of irrelevant literature,poor quality and obsolete literature,77 documents were finally included for review. RESULTS AND CONCLUSION:Flap ischemia/reperfusion injury may be related to pathological factors such as inflammatory response,oxidative stress response,Ca2+overload,and apoptosis,which can cause apoptosis of vascular endothelial cells,vascular damage and microcirculation disorders in the flap,and eventually lead to flap necrosis.Studies have found that mesenchymal stem cell transplantation,platelet-rich plasma,signaling pathway modulators,shock waves,and pretreatment can alleviate flap ischemia/reperfusion injuries from different aspects and to varying degrees,and reduce the necrosis rate and necrosis area of the grafted flap.Although there are many therapeutic methods for skin flap ischemia/reperfusion injury,a unified and effective therapeutic method has not yet been developed in the clinic,and the advantages and disadvantages of various therapeutic methods have not yet been compared.Most of the studies remain in the stage of animal experiments,rarely involving clinical observations.Therefore,a lot of research is required in the future to gradually move from animal experiments to the clinic in order to better serve the clinic.

Background During pregnancy, negative emotions such as anxiety and depression may induce cortisol disruption. Cortisol can be transmitted to the fetus through the placental barrier, thereby affecting the neurodevelopment of the offspring. Objective To investigate the relationship between placental cortisol, maternal depression during pregnancy, and neurodevelopment of 3-month-old infants. Methods From September 2022 to September 2023, 171 pregnant women ordered routine prenatal checks at the obstetrics outpatient department of a tertiary hospital in Ningxia were selected using a prospective cohort design. After providing informed consent, these women participated in a questionnaire survey that covered general individual characteristics, prenatal depression, and sleep quality. At birth, placental samples were collected to measure cortisol levels using ELISA kits. Follow-up assessments on the neurodevelopmental of 3-month-old infants were conducted using the Warning Sign for Children Mental and Behavioral Development. LASSO regression analysis was conducted to screen the influencing factors of depression during pregnancy. Huber regression analysis was then applied to assess potential linear relationship between depression during pregnancy and placental cortisol levels. Log-binomial regression was used to analyze the linear relationships between cortisol levels and neurodevelopmental delay in 3-month-old infants. Additionally, a mediation effect model was fitted using R 4.3.3 to assess possible mediating role of cortisol in the association between prenatal depression and neurodevelopmental delay in 3-month-old infants. Results The positive rate of prenatal depression was 33.33%. Nine factors affecting prenatal depression were identified by LASSO regression, including rural residence, high school education or above, extroverted personality characteristics, moderate early pregnancy reactions, baby sex expectation, prenatal anxiety, family dysfunction, exposure to stressful life events during pregnancy, and moderate prenatal sleep quality. The Huber regression model showed a positive linear correlation between prenatal depression and placental cortisol (P<0.05). With or without controlling confounding factors, the results of log-binomial regression modeling showed that cortisol levels were associated with a reduced risk of neurodevelopmental delay in 3-month-old infants (crude model: RR=0.988, 95%CI: 0.9768, 0.9996, P＜0.05; adjusted model: RR=0.988, 95%CI: 0.9764, 0.9993, P＜0.05). A mediating effect of placental cortisol between prenatal depression and the risk of neurodevelopmental delay in 3-month-old offspring was found statistically significant (P=0.045), accounting for 67.0% of the total effect. Conclusion Prenatal depression is associated with elevated placental cortisol levels, and higher cortisol levels are found to be related to a lower risk of neurodevelopmental delay in infants. Placental cortisol mediates the relationship between prenatal depression and infant neurodevelopment.

ObjectiveTo identify the patients with metabolic dysfunction-associated fatty liver disease （MAFLD） among the health check-up population， and to perform stratified management of patients with the low， medium， and high risk of advanced fibrosis based on noninvasive fibrosis scores. MethodsA cross-sectional study was conducted among 3 125 individuals who underwent physical examination in Beijing Physical Examination Center from December 2017 to December 2019， and they were divided into MAFLD group with 1 068 individuals and non-MAFLD group with 2 057 individuals. According to BMI， the MAFLD group was further divided into lean MAFLD group （125 individuals with BMI<24 kg/m²） and non-lean MAFLD group （943 individuals with BMI≥24 kg/m²）. Indicators including demographic data， past history， laboratory examination， and liver ultrasound were compared between groups. Fibrosis-4 （FIB-4） score， NAFLD fibrosis score （NFS）， aspartate aminotransferase-to-platelet ratio index （APRI）， and BARD score were calculated for the patients in the MAFLD group to assess the risk of advanced fibrosis. The independent-samples t test was used for comparison of normally distributed continuous data between two groups， and the Mann-Whitney U rank sum test was used for comparison of non-normally distributed continuous data between two groups； the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. A logistic regression analysis was used to investigate the influence of each indicator in MAFLD. ResultsCompared with the non-MAFLD group， the MAFLD group had significantly higher age （Z=-9.758， P<0.05）， proportion of male patients （χ²=137.555， P<0.05）， and levels of body weight （Z=-27.987， P<0.05）， BMI （Z=-32.714， P<0.05）， waist circumference （Z=-31.805， P<0.05）， hip circumference （Z=-26.342， P<0.05）， waist-hip ratio （Z=-28.554， P<0.05）， alanine aminotransferase （ALT） （Z=-25.820， P<0.05）， aspartate aminotransferase （AST） （Z=-16.894， P<0.05）， gamma-glutamyl transpeptidase （GGT） （Z=-25.069， P<0.05）， alkaline phosphatase （Z=-12.533， P<0.05）， triglyceride （Z=-27.559）， total cholesterol （Z=-7.833， P<0.05）， low-density lipoprotein cholesterol （LDL-C） （Z=-8.222， P<0.05）， and uric acid （UA） （Z=-20.024， P<0.05）， as well as a significantly higher proportion of patients with metabolic syndrome （MetS） （χ²=578.220， P<0.05）， significantly higher prevalence rates of hypertension （χ²=241.694， P<0.05）， type 2 diabetes （χ²=796.484， P<0.05）， and dyslipidemia （χ²=369.843， P<0.05）， and a significant reduction in high-density lipoprotein cholesterol （HDL-C） （Z=23.153， P<0.001）. The multivariate logistic regression analysis showed that male sex （odds ratio ［OR］=1.45， 95% confidence interval ［CI］： 1.203‍ ‍—‍ ‍1.737）， ALT （OR=1.05， 95%CI： 1.046‍ ‍—‍ ‍1.062）， LDL-C （OR=1.23， 95%CI： 1.102‍ ‍—‍ ‍1.373）， and comorbidity with MetS （OR=5.97， 95%CI： 4.876‍ ‍—‍ ‍7.316） were independently associated with MAFLD. Compared with the non-lean MAFLD group， the lean MAFLD group had significantly higher age （Z=3.736， P<0.05） and HDL-C （Z=2.679， P<0.05） and significant reductions in the proportion of male patients （χ²=28.970， P<0.05）， body weight （Z=-14.230， P<0.05）， BMI （Z=-18.188， P<0.05）， waist circumference （Z=-13.451， P<0.05）， hip circumference （Z=-13.317， P<0.05）， ALT （Z=-4.519， P<0.05）， AST （Z=-2.258， P<0.05）， GGT （Z=-4.592， P<0.05）， UA （Z=-4.415， P<0.05）， the proportion of patients with moderate or severe fatty liver disease or MetS （χ²=42.564， P<0.05）， and the prevalence rates of hypertension （χ²=12.057， P<0.05） and type 2 diabetes （χ²=3.174， P<0.05）. Among the patients with MAFLD， 10 patients （0.9%） had an FIB-4 score of >2.67， 4 patients （0.4%） had an NFS score of >0.676， 8 patients （0.7%） had an APRI of >1， and 551 patients （51.6%） had a BARD score of ≥2. ConclusionThere is a relatively high prevalence rate of MAFLD among the health check-up population in Beijing， but with a relatively low number of patients with a high risk of advanced fibrosis， and such patients need to be referred to specialized hospitals for liver diseases.

The classic formula Fangji Fulingtang is from ZHANG Zhongjing's Synopsis of the Golden Chamber in the Eastern Han dynasty. It is composed of Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma， with the effects of reinforcing Qi and invigorating spleen， warming Yang and promoting urination. By a review of ancient medical books， this paper summarizes the composition， original plants， processing， dosage， decocting methods， indications and other key information of Fangji Fulingtang， aiming to provide a literature basis for the research， development， and clinical application of preparations based on this formula. Synonyms of Fangji Fulingtang exist in ancient medical books， while the formula composition in the Synopsis of the Golden Chamber is more widespread and far-reaching. In this formula， Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma are the dried root of Stephania tetrandra， the dried root of Astragalus embranaceus var. mongholicus， the dried shoot of Cinnamomum cassia， the dried sclerotium of Poria cocos， and the dried root and rhizome of Glycyrrhiza uralensis， respectively. Fangji Fulingtang is mainly produced into powder， with the dosage and decocting method used in the past dynasties basically following the original formula. Each bag is composed of Stephaniae Tetrandrae Radix 13.80 g， Astragali Radix 13.80 g， Cinnamomi Ramulus 13.80 g， Poria 27.60 g， and Glycyrrhizae Radix et Rhizoma 9.20 g. The raw materials are purified， decocted in water from 1 200 mL to 400 mL， and the decoction should be taken warm， 3 times a day. Fangji Fulingtang was originally designed for treating skin edema， and then it was used to treat impediment in the Qing dynasty. In modern times， it is mostly used to treat musculoskeletal and connective tissue diseases and circulatory system diseases， demonstrating definite effects on various types of edema and heart failure. This paper clarifies the inheritance of Fangji Fulingtang and reveals its key information （attached to the end of this paper）， aiming to provide a theoretical basis for the development of preparations based on this formula.

The classic formula Fangji Fulingtang is from ZHANG Zhongjing's Synopsis of the Golden Chamber in the Eastern Han dynasty. It is composed of Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma， with the effects of reinforcing Qi and invigorating spleen， warming Yang and promoting urination. By a review of ancient medical books， this paper summarizes the composition， original plants， processing， dosage， decocting methods， indications and other key information of Fangji Fulingtang， aiming to provide a literature basis for the research， development， and clinical application of preparations based on this formula. Synonyms of Fangji Fulingtang exist in ancient medical books， while the formula composition in the Synopsis of the Golden Chamber is more widespread and far-reaching. In this formula， Stephaniae Tetrandrae Radix， Astragali Radix， Cinnamomi Ramulus， Poria， and Glycyrrhizae Radix et Rhizoma are the dried root of Stephania tetrandra， the dried root of Astragalus embranaceus var. mongholicus， the dried shoot of Cinnamomum cassia， the dried sclerotium of Poria cocos， and the dried root and rhizome of Glycyrrhiza uralensis， respectively. Fangji Fulingtang is mainly produced into powder， with the dosage and decocting method used in the past dynasties basically following the original formula. Each bag is composed of Stephaniae Tetrandrae Radix 13.80 g， Astragali Radix 13.80 g， Cinnamomi Ramulus 13.80 g， Poria 27.60 g， and Glycyrrhizae Radix et Rhizoma 9.20 g. The raw materials are purified， decocted in water from 1 200 mL to 400 mL， and the decoction should be taken warm， 3 times a day. Fangji Fulingtang was originally designed for treating skin edema， and then it was used to treat impediment in the Qing dynasty. In modern times， it is mostly used to treat musculoskeletal and connective tissue diseases and circulatory system diseases， demonstrating definite effects on various types of edema and heart failure. This paper clarifies the inheritance of Fangji Fulingtang and reveals its key information （attached to the end of this paper）， aiming to provide a theoretical basis for the development of preparations based on this formula.

OBJECTIVE To evaluate the quality of Mongolian medicine Sendeng-4 based on qualitative and quantitative analysis combined with chemical pattern recognition， in order to provide the reference for its quality control. METHODS The chemical components in Sendeng-4 were analyzed qualitatively by HPLC-Q-Exactive-MS. The contents of 16 components （methyl gallate， ethyl gallate， epicatechin， dihydromyricetin， genipin-1-O-β-D-gentiobioside， caffeic acid， catechin， corilagin， deacetylasperulosidic acid methyl ester， rutin， geniposide， luteolin， myricetin， quercetin， ferulic acid， and toosendanin） in 15 batches of Sendeng-4 （sample S1-S15） were quantitatively analyzed by HPLC-MS/MS. Cluster analysis （CA）， principal component analysis （PCA）， and orthogonal partial least squares discriminant analysis were conducted and variable importance projection （VIP） value greater than 1 was used as the index to screen the differential components. RESULTS A total of 73 chemical components were identified in Sendeng-4， including 20 flavonoids， 16 tannins， 14 organic acids， etc. According to the quantitative analysis， the results exhibited that the average contentsthe of above 16 components in 15 batches of Sendeng-4 were 3.683-7.730， 2.391-6.952， 2 275.538-4 377.491， 2 699.188-3 537.924， 858.266-1 377.393， 3.366-11.003， 140.624-315.683，414.629-978.334， 285.501-1 510.457， 27.799-48.325， 3 625.415-6 309.563， 0.506-0.656， 442.337-649.283， 47.093-59.736， 12.942-15.822， 127.738-326.649 μg/g， respectively. According to the results of CA and PCA， 15 batches of samples could be clustered into two categories: S1-S3， S5-S6， S9-S10 and S13 were clustered into one category； S4， S7-S8， S11-S12， S14-S15 were clustered into one category. VIP values of geniposide， epicatechin， deacetylasperulosidic acid methyl ester and genipin-1-O- β-D-gentiobioside were all greater than 1. CONCLUSIONS HPLC-Q-Exactive-MS and HPLC-MS/MS techniques are employed for the qualitative and quantitative analysis of Sendeng-4. Through chemical pattern recognition analysis， four differential components are identified: geniposide， epicatechin， deacetylasperulosidic acid methyl ester， and genipin-1-O-β-D-gentiobioside.

ObjectiveTo investigate the mechanism of action of Bushen Huoxue prescription （BSHXP） in regulating premature ovarian failure in rats through the PTEN-induced kinase 1 （PINK1）/Parkinson's protein （Parkin） signaling pathway-mediated mitophagy. MethodsA total of 48 rats were randomly divided into a blank group consisting of eight rats， while the remaining 40 rats underwent modeling. The modeling group was intraperitoneally injected with 4 mg·kg^-1 cisplatin solution， followed by a second injection one week later， for a total of two injections. The estrous cycle was observed through vaginal smears for 14 consecutive days to determine whether the modeling was successful. The successfully modeled rats were randomly divided into a model group， groups receiving low， medium， and high doses of BSHXP at 9.72， 19.44， and 38.88 g·kg^-1·d^-1 （BSHXP-L， BSHXP-M， and BSHXP-H groups）， and a positive control group treated with estradiol valerate （0.09 mg·kg^-1·d^-1）， for 21 consecutive days. The body weight of the rats was measured weekly. After the final administration， rats were anesthetized， and their blood and ovaries were collected. The ovarian weight was measured. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of anti-Müllerian hormone （AMH）， follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， and estradiol （E₂）. Assay kits were used to measure the levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in the rat serum. Hematoxylin-eosin （HE） staining was used to observe the morphological changes in the ovaries. Immunohistochemistry （IHC） was performed to detect microtubule autophagy-related protein 1 light chain 3B（LC3B） protein expression in ovarian tissue， and electron microscopy was employed to examine the mitochondrial and autophagosome changes in the rat ovaries. Western blot was used to detect the protein expression of PINK1， Parkin， LC3B， and p62. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of PINK1， Parkin， LC3B， and p62 in ovarian tissue. ResultsCompared with the blank group， the model group showed significant reductions in body weight， weight gain， and ovarian weight （P<0.01）， along with decreased serum AMH and E₂ levels （P<0.01）， while FSH and LH levels were increased （P<0.01）. Serum MDA levels were significantly increased （P<0.01）， and SOD levels were significantly reduced （P<0.01）. The ovarian tissue structure was disordered， and the zona pellucida was wrinkled into an irregular acidophilic annular object， accompanied by an increased number of closed follicles. Electron microscopy showed mitochondrial swelling， unclear structure， and no obvious autophagosomes and autolysosome structures. The proteins and mRNA expression levels of PINK1， Parkin， LC3B， and p62 in the ovarian tissue were significantly reduced （P<0.01）. Compared with the model group， all treatment groups showed varying degrees of increases in body weight and ovarian weight （P<0.05， P<0.01）. Except for the BSHXP-L group， all treatment groups showed increased body weight gain （P<0.01）. All treatment groups showed significantly increased serum AMH and decreased FSH levels （P<0.01）. Except for the BSHXP group， all treatment groups showed varying degrees of increase and decrease in serum E₂ and LH levels （P<0.05， P<0.01）. All treatment groups showed reduced serum MDA levels （P<0.01）， while the BSHXP-M， BSHXP-H， and the positive control groups demonstrated improved serum SOD levels （P<0.05， P<0.01）. All treatment groups showed an increased number of follicles at all stages， visible mature follicles， and a decreased number of closed follicles. Electron microscopy showed relieved mitochondrial swelling， morphology close to normal， clear structure， and visible formation of autolysosomes in all treatment groups. Additionally， the protein and mRNA expression levels of PINK1， Parkin， LC3B， and p62 in ovarian tissue were significantly increased （P<0.05， P<0.01）. ConclusionBSHXP may improve ovarian function in rats with premature ovarian failure by regulating the PINK1/Parkin signaling pathway， activating mitochondrial autophagy， and reducing oxidative damage.

ObjectiveTo investigate the mechanism of action of Bushen Huoxue prescription （BSHXP） in regulating premature ovarian failure in rats through the PTEN-induced kinase 1 （PINK1）/Parkinson's protein （Parkin） signaling pathway-mediated mitophagy. MethodsA total of 48 rats were randomly divided into a blank group consisting of eight rats， while the remaining 40 rats underwent modeling. The modeling group was intraperitoneally injected with 4 mg·kg^-1 cisplatin solution， followed by a second injection one week later， for a total of two injections. The estrous cycle was observed through vaginal smears for 14 consecutive days to determine whether the modeling was successful. The successfully modeled rats were randomly divided into a model group， groups receiving low， medium， and high doses of BSHXP at 9.72， 19.44， and 38.88 g·kg^-1·d^-1 （BSHXP-L， BSHXP-M， and BSHXP-H groups）， and a positive control group treated with estradiol valerate （0.09 mg·kg^-1·d^-1）， for 21 consecutive days. The body weight of the rats was measured weekly. After the final administration， rats were anesthetized， and their blood and ovaries were collected. The ovarian weight was measured. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of anti-Müllerian hormone （AMH）， follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， and estradiol （E₂）. Assay kits were used to measure the levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in the rat serum. Hematoxylin-eosin （HE） staining was used to observe the morphological changes in the ovaries. Immunohistochemistry （IHC） was performed to detect microtubule autophagy-related protein 1 light chain 3B（LC3B） protein expression in ovarian tissue， and electron microscopy was employed to examine the mitochondrial and autophagosome changes in the rat ovaries. Western blot was used to detect the protein expression of PINK1， Parkin， LC3B， and p62. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of PINK1， Parkin， LC3B， and p62 in ovarian tissue. ResultsCompared with the blank group， the model group showed significant reductions in body weight， weight gain， and ovarian weight （P<0.01）， along with decreased serum AMH and E₂ levels （P<0.01）， while FSH and LH levels were increased （P<0.01）. Serum MDA levels were significantly increased （P<0.01）， and SOD levels were significantly reduced （P<0.01）. The ovarian tissue structure was disordered， and the zona pellucida was wrinkled into an irregular acidophilic annular object， accompanied by an increased number of closed follicles. Electron microscopy showed mitochondrial swelling， unclear structure， and no obvious autophagosomes and autolysosome structures. The proteins and mRNA expression levels of PINK1， Parkin， LC3B， and p62 in the ovarian tissue were significantly reduced （P<0.01）. Compared with the model group， all treatment groups showed varying degrees of increases in body weight and ovarian weight （P<0.05， P<0.01）. Except for the BSHXP-L group， all treatment groups showed increased body weight gain （P<0.01）. All treatment groups showed significantly increased serum AMH and decreased FSH levels （P<0.01）. Except for the BSHXP group， all treatment groups showed varying degrees of increase and decrease in serum E₂ and LH levels （P<0.05， P<0.01）. All treatment groups showed reduced serum MDA levels （P<0.01）， while the BSHXP-M， BSHXP-H， and the positive control groups demonstrated improved serum SOD levels （P<0.05， P<0.01）. All treatment groups showed an increased number of follicles at all stages， visible mature follicles， and a decreased number of closed follicles. Electron microscopy showed relieved mitochondrial swelling， morphology close to normal， clear structure， and visible formation of autolysosomes in all treatment groups. Additionally， the protein and mRNA expression levels of PINK1， Parkin， LC3B， and p62 in ovarian tissue were significantly increased （P<0.05， P<0.01）. ConclusionBSHXP may improve ovarian function in rats with premature ovarian failure by regulating the PINK1/Parkin signaling pathway， activating mitochondrial autophagy， and reducing oxidative damage.

Objective: To investigate the distribution characteristics of CD36 antigen in healthy individuals in Xinjiang, China and analyze the molecular mechanisms underlying CD36 deficiency. Methods: Flow cytometry was used to assess CD36 antigen expression on platelets from 881 healthy individuals who underwent physical examinations between June and August 2023. Differences in CD36 antigen distribution among ethnic groups were compared, and genotyping and third-generation sequencing were conducted on samples with CD36 deficiency. Results: Among the 881 samples, 4 cases (0.5%) of CD36 type Ⅱ deficiency were identified. The deficiency frequency was 0.7% (3/430) in Han individuals and 0.3% (1/363) in Uygur individuals, with no statistically significant difference between the two groups (P>0.05). No mutations were detected in the coding regions of the deficient samples. Two samples exhibited a (TG)11 in intron 3. Among the 12 linked mutation sites, g. 55589 G>A was mutated to g. 55589G Del, while g. 55593 A del did not occur; however, g. 55591A>T was observed nearby. Additionally, 52742insGAAAA was present in 100% of the (TG)11 haplotypes, potentially representing a novel linked mutation. Conclusion: This study indicates that the positive frequency of CD36 antigen in Xinjiang is relatively high, suggesting a low risk of alloimmune diseases in clinical practice. The (TG)11 in intron 3 is not universally present in all CD36 type Ⅱ deficiency cases, and the number of linked mutation sites extends beyond the previously reported 12.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.