PeerJ
·
2022
·
IF 3.061
Jinhuang Shen,Xinhua Ma,Yubin He,Yanjun Wang,Tianhua Zhong,Yonghong Zhang
Background Ulcerative colitis is a unique inflammatory bowel disease with ulcerative lesions of the colonic mucosa. Melianodiol (MN), a triterpenoid, isolated from the fruits of the Chinese medicinal plant Melia azedarach , possesses significant anti-inflammatory properties. Objective The present study investigated the protective effects of MN on lipopolysaccharide (LPS)-induced macrophages and DSS-mediated ulcerative colitis in mice. Methods In the study, mice were given MN (50, 100, and 200 mg/kg) and 5-ASA (500 mg/kg) daily for 9 days after induction by DSS for 1 week. The progress of the disease was monitored daily by observation of changes in clinical signs and body weight. Results The results showed that MN effectively improved the overproduction of inflammatory factors (IL-6, NO, and TNF- α ) and suppressed the activation of the NF- κ B signalling cascade in LPS-mediated RAW264.7 cells. For DSS-mediated colitis in mice, MN can reduce weight loss and the disease activity index (DAI) score in UC mice, suppress colon shortening, and alleviate pathological colon injury. Moreover, MN treatment notably up regulated the levels of IL-10 and down regulated those of IL-1 β and TNF- α , and inhibited the protein expression of p-JAK2, p-STAT3, iNOS, NF- κ B P65, p-P65, p-IKK α/β , and p-I κ B α in the colon. After MN treatment, the levels of MDA and NO in colonic tissue were remarkably decreased, whereas the levels of GSH, SOD, Nrf-2, Keap-1, HO-1, I κ B α , and eNOS protein expression levels were significantly increased. Conclusion These results indicate that MN can activate the Nrf-2 signalling pathway and inhibit the JAK/STAT, iNOS/eNOS, and NF- κ B signalling cascades, enhance intestinal barrier function, and effectively reduce the LPS-mediated inflammatory response in mouse macrophages and DSS-induced intestinal injury in UC.
研究领域:
药理学
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免疫学
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胃肠病学
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DOI
PubMed
高影响因子
IMMUNOBIOLOGY
·
2023
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IF 2.8
Zepeng Chen,Qinglong Gu,Ruichao Chen
Ulcerative colitis (UC) is a chronic inflammatory disease affecting the colon that can be influenced by microRNAs (miRNAs). This study aims to investigate the impact of miR-146a-5p on lipopolysaccharide (LPS)-induced Caco-2/HT-29 cell autophagy and NLRP3 inflammasome activation and the underlying mechanism, with the aim of identifying potential therapeutic targets. We used LPS to establish Caco-2/HT-29 cell models and measured cell viability by CCK-8. The levels of miR-146a-5p, RNF8, markers of NLRP3 inflammasome activation and autophagy, proteins involved in the Notch1/mTORC1 pathway, and inflammatory factors were assessed by RT-qPCR, Western blot, and ELISA. Intestinal epithelial barrier function was evaluated by measuring transepithelial electrical resistance. Autophagic flux was measured using tandem fluorescent-labeled LC3. miR-146a-5p was highly-expressed in LPS-induced Caco-2/HT-29 cells, and autophagy flux was blocked at the autolysosomal stage after LPS induction. Inhibition of miR-146a-5p suppressed NLRP3 inflammasome activation, reduced intestinal epithelial barrier damage, and facilitated autophagy inhibition in LPS-induced Caco-2/HT-29 cells. The autophagy inhibitor NH4Cl partially nullified the inhibitory effects of miR-146a-5p inhibition on NLRP3 inflammation activation. miR-146a-5p targeted RNF8, and silencing RNF8 partly abrogated the action of miR-146a-5p inhibition on promoting autophagy and inhibiting NLRP3 inflammasome activation. miR-146a-5p inhibition suppressed the Notch1/mTORC1 pathway activation by upregulating RNF8. Inhibition of the Notch1/mTORC1 pathway partially nullified the function of silencing RNF8 on inhibiting autophagy and bolstering NLRP3 inflammasome activation. In conclusion, miR-146a-5p inhibition may be a potential therapeutic approach for UC, as it facilitates autophagy of LPS-stimulated Caco-2/HT-29 cells, inhibits NLRP3 inflammasome activation, and reduces intestinal epithelial barrier damage by upregulating RNF8 and suppressing the Notch1/mTORC1 pathway.
研究领域:
炎症性肠病
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分子生物学
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细胞生物学
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药理学
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DOI
PubMed
高影响因子
MOLECULES
·
2022
·Vol. 27
·期 24
·8816
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IF 4.927
Yeye Du,Shuangjie Zhu,Ran Wang,Xingyong Chen,Kezhou Cai
This study was designed to isolate an anti-inflammatory activity oligopeptide from goose blood (GBP) for ameliorating LPS-mediated inflammation response and oxidative stress in RAW264.7 macrophages. In this study, GBP was isolated by tangential flow ultrafiltration system (TFUS) combined with size exclusion chromatography (SEC), ion exchange chromatography (IEC), and reversed-phase liquid chromatography (RP-LC), and then identified by liquid chromatography mass spectrometry (LC–MS/MS). The experiment results indicated that the amino acid sequence of oligopeptide with the best anti-inflammatory activity was IIe-Val-Tyr-Pro-Trp-Thr-Gln-Arg (IVYPWTQR), which had a molecular weight of 1062.5720 Da, and was derived from haemoglobin subunit beta OS in goose blood. In addition, IVYPWTQR was confirmed to have satisfactory stability and maintained high anti-inflammatory activity in a simulated gastrointestinal digestion. The mechanism by which the IVYPWTQR protected against LPS-mediated inflammation response was attributed to downregulating theTLR4/NF-kB/iNOSpathway. Moreover, IVYPWTQR ameliorated oxidative stress damage in inflammatory state was attributed to activating antioxidant defence system, which was regulated byKeap-1/NRF2/HO-1signalling pathway for decreasing the accumulation of reactive oxide species (ROS). In summary, these results indicated GBP could serve as a potential functional factor for prevention and improvement of inflammation mediated by LPS and provided an affordable dietary intervention strategy to prevent inflammation.Keywords:goose blood;bioactive peptides;anti-inflammatory;digestive stability
研究领域:
免疫学
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药理学
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生物化学
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细胞生物学
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
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2026
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IF 5.7
Zhen Zhou,Yongfen Bao,Rongjie Li,Rui Yang,Qingyu Peng,Tianci Lu,Binyu Wang,Ming Zhang,Jie Xu,Ying Xiang,Shigang Shan,Liqiong Huang
Background Preeclampsia (PE) is a severe hypertensive disorder in pregnancy, and disruption of placental energy homeostasis, particularly mitochondrial dysfunction, plays a critical role in its pathogenesis. Melatonin (MEL) and Metformin (MET), an effect associated through the AMP-activated protein kinase/Sirtuin 3 (AMPK/SIRT3) signaling pathway. However, the precise mechanisms remain unclear. Materials and methods The PE rat model was established in Sprague–Dawley (SD) rats by lipopolysaccharide (LPS) injection after confirmation of pregnancy. Pathological changes, protein expression, inflammatory and angiogenic factors, and mitochondrial status in placental tissue and HTR-8/SVneo trophoblasts were assessed by histology, immunohistochemistry, Western blotting, ELISA, RT-qPCR, reactive oxygen species (ROS) detection, transmission electron microscopy, and measurements of mitochondrial membrane potential and cytosolic calcium. Results Both MEL and MET individually activated the AMPK/SIRT3 signaling pathway, thereby enhancing mitochondrial function and placental energy homeostasis, while attenuating LPS-induced oxidative stress and inflammatory damage in placental tissue and trophoblast cells. Conclusions MEL and MET, when administered together, improve placental mitochondrial dysfunction and inflammatory injury in PE, which is associated with activation of the AMPK/SIRT3 signaling pathway, suggesting a potential therapeutic strategy for preeclampsia using clinically available agents.
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 5.4
Jinni Meng,Ping Wei,Heping Yang,Lin Chen,Cheng Peng,Ou Dai,Qinmei Zhou,Liang Xiong
Ethnopharmacological relevance Ligusticum chuanxiong Hort. (Chuanxiong) is a traditional Chinese medicinal herb whose rhizome has been historically and clinically used to treat conditions such as headache, dizziness, and depression. These traditional application broadly correlate with modern diagnoses of cerebrovascular dysfunction, impaired cerebral blood flow, and neuroinflammation. As a characteristic phthalide dimer and major bioactive constituent of Chuanxiong, levistilide A (LA) has shown significant therapeutic potential. However, its specific antidepressant and anxiolytic properties require further clarification. Aim of the study This study aimed to assess the efficacy of LA against depression and anxiety, with the further goal of elucidating its underlying molecular mechanisms. Materials and methods A depression- and anxiety-like state was induced in C57BL/6 mice by LPS challenge after which they received therapeutic intervention with different doses of LA. The therapeutic efficacy was assessed by behavioral tests, histopathological analyses, and enzyme-linked immunosorbent assays (ELISA). Concurrently, we assessed microglial activation via immunofluorescence, along with mitochondrial status by measuring reactive oxygen species (ROS) levels with flow cytometry and examining ultrastructure with transmission electron microscopy (TEM). To investigate the cellular mechanisms, LPS-stimulated BV2 cells was established . In this model, autophagic flux was quantitatively measured using Bafilomycin A1 (Baf A1) inhibition assays combined with western blot analysis of LC3B-II. And mitophagy was evaluated by co-immunofluorescence LC3B with the mitochondrial marker Tomm40 in both BV2 cells and mouse hippocampal CA3. Building on this, computational approaches, along with experimental methodologies including immunofluorescence and western blotting, were utilized to elucidate the underlying molecular mechanisms. Furthermore, SIRT3-specific siRNA ( siRNA -SIRT3) was used for further validation. Results The LA treatment demonstrated a notable protective role against LPS-induced depression and anxiety through ameliorating behaviors accompanied by depression- and anxiety-like behaviors, attenuating neuronal damage, downregulating pro-inflammatory cytokine expression levels, and suppressing microglial overactivation. Mechanistically, LA alleviated oxidative stress and mitochondrial dysfunction by reducing ROS accumulation and mitigating mitochondrial damage. In the LPS-induced BV2 cells, LA treatment significantly enhanced autophagic flux, as evidenced by the further accumulation of LC3B-II upon Baf A1 inhibition, which confirmed the promotion of functional autophagy. Concurrently, the increased co-localization of Tomm40 with LC3B upon LA treatment provided direct evidence for mitophagy activation. Molecular docking combined with molecular dynamics simulation analyses revealed robust binding interactions between LA and SIRT3, as well as between SIRT3 and PINK1. Further investigation into the downstream pathway revealed that LA effectively activated the SIRT3/PINK1/Parkin pathway. This was supported by the western blot analyses. Specifically, LA treatment increased the SIRT3, PINK1, Parkin, and LC3B-II expression levels, while it decreased p62 levels. This result suggested mitophagy activation. An immunofluorescence analysis corroborated this result and revealed increased cytoplasmic colocalization of Tomm40 with LC3B following the LA treatment. Consistent with these findings, LA significantly suppressed neuroinflammation in LPS-stimulated BV2 microglial cells by inhibiting both NO production and the release of pro-inflammatory cytokines.. Importantly, LA recapitulated its favorable impacts on mitochondrial function and the SIRT3/PINK1/Parkin signaling cascade in this cellular model. The functional necessity of this pathway was demonstrated by the findings that SIRT3 knockdown with siRNA -SIRT3 in BV2 cells abolished regulatory impact of LA on PINK1/Parkin pathway proteins. Conclusions LA serves as a potential therapeutic agent for depression and anxiety through activating mitophagy mediated by the SIRT3/PINK1/Parkin pathway. The results of this study provide scientific evidence for the clinical application of LA in treating depression and anxiety.
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DOI
PubMed
高影响因子
MEDIATORS OF INFLAMMATION
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2026
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IF 4.9
Haipeng Tang,Zhiliang Sun,Weibo Qin,Guangzhi Cai,Wenyi Gao,Yang Wang,Jiyu Gong
Zhuye Shigao Decoction (ZSD), a classic traditional Chinese medicine (TCM) formula, has demonstrated therapeutic efficacy in clinical settings for acute pneumonia; however, its mechanism of action remains elusive. This study aims to investigate the therapeutic effects and potential mechanisms of ZSD in lipopolysaccharide (LPS)‐induced acute pneumonia in mice. A liquid chromatography‐mass spectrometry (LC‐MS)‐based metabolomics approach, integrated with a gene expression omnibus (GEO) data mining technique, was employed in this investigation. The results indicated that ZSD administration significantly alleviated LPS‐induced pathological changes in lung tissue. In the model group, the concentrations of interleukin‐1 β (IL‐1 β ), interleukin‐6 (IL‐6), and tumor necrosis factor‐ α (TNF‐ α ) were increased, whereas the levels of immunoglobulin A (IgA) and immunoglobulin M (IgM) were significantly decreased. These indicators were reversed considerably in the ZSD‐high dose (ZSD‐H) group. A total of 118 metabolites exhibiting significant alterations in lung tissue were identified through metabolomics analysis. Following ZSD treatment, 84 of these metabolites were negatively regulated, and the associated metabolic processes implicated multiple pathways, including sphingolipid and arachidonic acid (AA) metabolism. Differentially expressed genes (DEGs) were identified through a comprehensive analysis of GEO datasets. Integrative pathway analysis identified signaling pathways associated with ZSD treatment effects in acute pneumonia. Notably, the Janus kinase/signal transducer and activator of transcription (JAK‐STAT) and Toll‐like receptor (TLR) signaling pathways emerged as critical contributors to these effects. This study indicates that ZSD can exert therapeutic effects on LPS‐induced acute pneumonia through a regulatory mechanism involving multiple components, targets, and pathways.
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2014
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IF 2.711
Xiaomin Xia,Chuanyang Su,Juanli Fu,Pu Zhang,Xiaoji Jiang,Demei Xu,Lihua Hu,Erqun Song,Yang Song
This study investigated the protective effect of α-lipoic acid (LA) on lipopolysaccharide (LPS)/ d -galactosamine ( d -GalN)-induced fulminant hepatic failure in mice. First, we found that LA markedly reduced LPS/ d -GalN-induced increases in serum ALT and AST activities, which were supplemented with histopathological examination, suggested that LA has a protective effect on this model of hepatic damage. Livers challenged with LPS/ d -GalN exhibited extensive areas of vacuolization with the disappearance of nuclei and the loss of hepatic architecture. On the contrary, these pathological alterations were ameliorated by LA treatment. Next, we found that ROS and TBARS levels were increased in LPS/ d -GalN treated liver homogenates , which were attenuated by LA administration. Consistently, decreases in hepatic CAT and GPx activities were observed in LPS/ d -GalN group and were significantly restored by LA administration. Moreover, pretreatment with LA markedly reduced LPS/ d -GalN-induced iNOS , COX-2, TNF-α, NF-κB, IL-1β and IL-6 expressions. Furthermore, our data showed that TUNEL-positive cells increased in LPS/ d -GalN-treated mice liver which was counteracted by LA administration. LPS/ d -GalN induced apoptosis of hepatocytes, as estimated by caspase 3, caspase 8 and caspase 9 activations. Also, the increasing of Bax and the decreasing of Bcl-2 expressions also supported LPS/ d -GalN induced apoptosis. Interestingly, LA marked relieved these apoptotic features. Taking together, our results indicated that LA plays an important role on LPS/ d -GalN-induced fulminant hepatic failure through its antioxidant, anti-inflammatory and anti-apoptotic activities.
研究领域:
肝病学
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药理学
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免疫学
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细胞生物学
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DOI
PubMed
高影响因子
JOURNAL OF CHEMICAL NEUROANATOMY
·
2024
·
IF 2.7
Lili Ma,Na Mi,Zhi Wang,Rui Bao,Jing Fang,Yajing Ren,Xiuzhi Xu,Hongjia Zhang,Ying Tang
Neuroinflammation associated with microglial activation plays a role in the development of Parkinson's disease (PD). The upregulation of interferon regulatory factor 8 (IRF8) in microglia following peripheral nerve injury has been observed to induce microglial activation. This suggests the potential therapeutic significance of IRF8 in PD. This research aims to explore the effects of IRF8 on the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model and lipopolysaccharide (LPS)-induced neuroinflammation, along with its underlying mechanisms. The study examines the differential expression of IRF8 and its effects on neuropathological changes using a PD mouse model and a PD model established from BV2 cells in vitro . IRF8 was found to be prominently expressed in the substantia nigra pars compacta (SNpc) region of PD mice and LPS-stimulated BV2 cells, while the expression of tyrosine hydroxylase (TH) and dopamine (DA) content in the SNpc region of PD mice was notably reduced. MPTP treatment and LPS stimulation intensified microglial activation, inflammation, and activation of the AMPK/mTOR signaling pathway in vivo and in vitro , respectively. Upon IRF8 silencing in the PD mouse and cell models, the knockdown of IRF8 ameliorated MPTP-induced behavioral deficits, increased the counts of TH and Nissl-positive neurons and DA content, reduced the number of Iba-1-positive microglia, and reduced the content of inflammatory factors, possibly by inhibiting the AMPK/mTOR signaling pathway. Similar outcomes were observed in the PD cell model. In conclusion, the suppression of IRF8 alleviates neuroinflammation through regulating microglial activation in PD models in vivo and in vitro by the AMPK/mTOR signaling pathway.
研究领域:
神经科学
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药理学
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细胞生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
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2021
·
IF 3.636
Wei Liu,Ling Zhang,Shuo Sun,Long-sheng Tang,Shi-min He,An-qi Chen,Li-na Yao,Da-Long Ren
As a natural extract, cordycepin has been shown to play important regulatory roles in many life activities. In the study, the effects of cordycepin on inflammatory responses and the underlying mechanisms was explored using a zebrafish model. In the model of LPS-induced inflammation, cordycepin was found to significantly inhibited the expression of pro-inflammatory cytokines such as tnf-α, il-1β, il-6, and il-8 . Using in vivo imaging model, cordycepin significantly inhibited fluorescent-labeled neutrophils migrating towards injury sites. Furthermore, results showed that the phosphorylation level of ERK protein dramatically decreased after cordycepin treatment. Meanwhile, the ERK inhibitor, PD0325901, significantly inhibited the expression of pro-inflammatory cytokines in LPS-induced inflammatory model and neutrophils migration in the caudal fin injury model. This study indicated the important roles of cordycepin in inhibiting LPS and injury-induced inflammation and preliminarily explained the role of ERK protein in this process.
研究领域:
免疫学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
Scientific Reports
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2021
·Vol. 11
·期 1
·1-12
·
IF 4.38
Li Huxiao,Xu Jianrong,Li Xiaotian,Hu Yi,Liao Yue,Zhou Wei,Song Zhongchen
Psoralen is one of the most effective ingredients extracted from the Chinese herb, Psoralea corylifolia L . Studies have found that psoralen has anti-inflammatory and estrogen-like effects; however, little research has been conducted to elucidate the mechanisms underlying these effects. Through the molecule docking assay, psoralen was found to have a better combination with ERα than ERβ. In human periodontal ligament cells, psoralen was found to upregulate the estrogen target genes (e.g., CTSD, PGR, TFF1 ) and down-regulate the expression of inflammatory cytokines (TNF-α, IL-1β, IL-6 and IL-8) stimulated by P. gingivalis LPS, as well as TLR4-IRAK4-NF-κb signaling pathway proteins. These effects were reversed by the ER antagonist ICI 182780. These results indicated that psoralen may exert anti-inflammatory effects as an agonist to ER, which could provide a theoretical basis for the use of psoralen for adjuvant therapy and prevention of periodontitis.
研究领域:
药理学
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牙科
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分子生物学
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产品关联
DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
·
2019
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IF 3.743
Yanke Lin,Shuai Wang,Zemin Yang,Lu Gao,Ziyue Zhou,Pei Yu,Baojian Wu
Bilirubin is an endogenous substance derived from heme catabolism. In this study, we aimed to assess the anti-inflammatory activity of bilirubin, and to determine the mechanism thereof. The anti-inflammatory activity of bilirubin was evaluated using lipopolysaccharide (LPS)-treated peritoneal macrophages (PMs) and Raw264.7 cells, and mice with alum-induced peritonitis. The mRNA and proteins of NOD-like receptor family pyrin domain containing 3 (Nlrp3) and inflammatory cytokines were determined using qPCR and Western blotting, respectively. Distribution of phosphorylated (p) p65 [a NF-κB (nuclear factor-κB) subunit] in the cytoplasm and nucleus were evaluated by immunofluorescence analysis and electrophoretic mobility shift assay. Bilirubin prior to LPS treatment decreased protein expressions of Nlrp3, pro-interleukin (IL)-1β and mature IL-1β in PMs, whereas bilirubin post LPS treatment showed no effects. Bilirubin prior to LPS treatment dose-dependently repressed expressions of Nlrp3 and IL-1β, and inhibited translocation of p-p65 to nucleus in Raw264.7 cells. Bilirubin treatment decreased myeloperoxidase activity and reduced the levels of inflammatory cytokines (i.e., IL-1β, TNFα and IL-6) in lavage fluid in mice with alum-induced peritonitis. This was accompanied by a lower mortality rate. In addition, the mRNAs of Nlr p3 and IL-1β in peritoneal exudates cells were decreased, and the levels of p-p65 and mature IL-1β proteins were reduced. In conclusion, bilirubin acted on inflammation and alleviated alum–induced peritonitis through inactivation of Nlrp3 inflammasome.
研究领域:
免疫学
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炎症
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药理学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL ENDODONTIC JOURNAL
·
2019
·Vol. 53
·期 1
·72-83
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IF 3.331
T. Ning,J. Shao,X. Zhang,X. Luo,X. Huang,H. Wu,S. Xu,B. Wu,D. Ma
Aim To comparatively evaluate changes in the proliferation and mineralization abilities of dental pulp stem cells (DPSCs) from juvenile and adult rats in a lipopolysaccharide (LPS)-induced inflammatory microenvironment to provide a theoretical basis for the age-related differences observed in DPSCs during repair of inflammatory injuries. Methodology DPSCs were isolated from juvenile (JDPSCs) and adult rats (ADPSCs), and senescence-associated β-galactosidase staining was used to compare senescence between JDPSCs and ADPSCs. Effects of LPS on JDPSCs and ADPSCs proliferation were investigated by cell counting kit-8 assays and flow cytometry. Alizarin red staining, quantitative reverse transcription polymerase chain reaction and Western blot assay were used to examine the effects of LPS on mineralization-related genes and proteins in JDPSCs and ADPSCs. Immunohistochemistry was used to compare interleukin-1β (IL-1β) and osteocalcin (OCN) expression in the pulpitis model. Unpaired Student's t -tests and one-way anova were used for statistical analysis. Results DPSCs were isolated from juvenile and adult rat dental pulp tissues. At low concentrations (0.1–1 μg mL −1 ), LPS significantly promoted the proliferation of JDPSCs ( P < 0.01) and ADPSCs ( P < 0.01 or P < 0.05), with the effect being stronger in JDPSCs than in ADPSCs. In addition, mineralized nodules and the expression of mineralization-related genes ( OCN , DSPP , ALP , BSP ) increased significantly after stimulation with LPS (0.5 μg mL −1 ) in JDPSCs and ADPSCs ( P < 0.01 or P < 0.05), and JDPSCs displayed a more obvious increase than ADPSCs. Western blots revealed OCN and ALP expression levels in JDPSCs treated with LPS were significantly upregulated ( P < 0.05); meanwhile, ALP expression in ADPSCs increased slightly but significantly ( P < 0.05), and OCN expression was not affected. Finally, IL-1β expression was significantly higher ( P < 0.05) and OCN expression was significantly lower ( P < 0.05) in the inflamed dental pulp of adult rats than in juvenile rats. Conclusions A certain degree of inflammatory stimulation promoted the proliferation and mineralization of DPSCs; however, this effect declined with age. The DPSCs of adult donors in an inflammatory microenvironment have a weaker repair ability than that of juvenile donors, who are better candidates for tissues damage repair.
研究领域:
牙科学
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干细胞生物学
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炎症
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细胞老化
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产品关联
DOI
PubMed
高影响因子
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