Griseofulvin was considered an effective agent for cancer therapy in past decades. Although the negative effects of griseofulvin on microtubule stability are known, the exact target and mechanism of action in plants remain unclear. Here, we used trifluralin, a well-known herbicide targeting microtubules, as a reference and revealed the differences in root tip morphology, reactive oxygen species production (ROS), microtubule dynamics, and transcriptome analysis between Arabidopsis treated with griseofulvin and trifluralin to elucidate the mechanism of root growth inhibition by griseofulvin. Like trifluralin, griseofulvin inhibited root growth and caused significant swelling of the root tip due to cell death induced by ROS. However, the presence of griseofulvin and trifluralin caused cell swelling in the transition zone (TZ) and meristematic zone (MZ) of root tips, respectively. Further observations revealed that griseofulvin first destroyed cortical microtubules in the cells of the TZ and early elongation zone (EZ) and then gradually affected the cells of other zones. The first target of trifluralin is the microtubules in the root MZ cells. Transcriptome analysis showed that griseofulvin mainly affected the expression of microtubule-associated protein (MAP) genes rather than tubulin genes, whereas trifluralin significantly suppressed the expression of αβ-tubulin genes. Finally, it was proposed that griseofulvin could first reduce the expression of MAP genes, meanwhile increasing the expression of auxin and ethylene-related genes to disrupt microtubule alignment in root tip TZ and early EZ cells, induce dramatic ROS production, and cause severe cell death, eventually leading to cell swelling in the corresponding zones and inhibition of root growth.

本试验旨在探讨饲粮添加猪去氧胆酸(HDCA)对小鼠生长、能量代谢及脂肪消化吸收的影响.选用20只3周龄C57BL雄性小鼠,分为对照组和HDCA组,分别饲喂基础饲粮和添加了1.5％HDCA的试验饲粮.试验期为10周.结果表明:与对照组相比,1)HDCA对小鼠的采食量和终末体重无显著影响(P>0.05),但显著降低了小鼠的体增重(P<0.05).此外,HDCA显著减少了小鼠的皮下脂肪组织含量(P<0.05);2)HDCA增加了25和4℃环境温度下小鼠的褐色脂肪组织(BAT)产热(P<0.05),并提高了小鼠白天和黑夜的基础代谢,表明HDCA提高了小鼠的能量代谢;3)HDCA极显著降低了小鼠粗脂肪表观消化率(P<0.01),从而极显著增加了小鼠粪便的粗脂肪含量和粪便能值(P<0.01);4)HDCA有降低小鼠胰腺胰脂酶相关基因胆盐刺激性脂酶(BSSL)、磷脂酶A2(PLA2)、甘油三酯脂酶(PTL)和胰脂酶相关蛋白1(PLRP1)和胰脂酶相关蛋白2(PLRP2)的mRNA相对表达量的趋势(0.05≤P<0.10).综上所述,饲粮添加1.5％的HDCA能够通过提高小鼠的能量代谢,减少小鼠对脂肪的消化吸收,从而降低小鼠的皮下脂肪组织含量和体增重.

Nutritional diarrhea and subsequent performance degradation in weaned piglets are major challenges for the pig industry. Bile acids (BA) can be added to the diet as emulsifiers. This experiment was conducted to investigate the effects of chenodeoxycholic acid (CDCA), a major primary BA, on growth performance, serum metabolic profiles and gut health in weaned piglets. A total of 72 healthy weaned piglets were randomly assigned to the control (CON) and the CDCA groups, which were feed a basal diet and the basal diet supplemented with 200 mg/kg CDCA for 30 d, respectively. Our results demonstrated that CDCA significantly increased final BW and average daily gain (ADG), decreased feed-to-gain (F:G) ratio and tended to reduce diarrhea incidence. In addition, CDCA increased the villus height-to-crypt depth (V:C) ratio, elevated goblet cell numbers and the expression of tight junction proteins, suggesting the enhancement of intestinal barrier function. As an emulsifier, CDCA increased jejunal lipase activity and the mRNA expression of pancreatic lipases. CDCA supplementation also altered the serum metabolic profiles, including increasing the levels of indole 3-acetic acid, N′-formylkynurenine and theobromine that were beneficial for gut health. Moreover, the relative abundance of 2 beneficial gut bacteria, Prevotella 9 and Prevotellaceae TCG-001, were increased, whereas the relative abundance of a harmful bacteria, Dorea, was decreased in the gut of weaned piglets supplemented with CDCA. Importantly, the altered serum metabolic profiles showed a strong correlation with the changed gut bacteria. In conclusion, CDCA improved the growth performance of weaned piglets by improving intestinal morphology and barrier function, and enhancing lipid digestion, accompanied by alterations of serum metabolic profiles, and changes in relative abundance of certain gut bacteria.

This study aimed to investigate the effects of conjugated linoleic acid (CLA) on intestinal epithelial barrier function and explore the underlying mechanisms. IPEC-J2 cells and mice were treated with different CLA isomers. The intestinal epithelial barrier function determined by transepithelial electrical resistance (TEER), the expression of tight junction proteins, and the involvement of G-protein coupled receptor 120 (GPR120), intracellular calcium ([Ca2+]i) and myosin light chain kinase (MLCK) were assessed. In vitro, c9, t11-CLA, but not t10, c12-CLA isomer, impaired epithelial barrier function in IPEC-J2 by downregulating the expression of tight junction proteins. Meanwhile, c9, t11-CLA isomer enhanced GPR120 expression, while knockdown of GPR120 eliminated the impaired epithelial barrier function induced by c9, t11-CLA isomer. In addition, c9, t11-CLA isomer increased [Ca2+]i and activated the MLCK signaling pathway in a GPR120-dependent manner. However, chelation of [Ca2+]i reversed c9, t11-CLA isomer-induced MLCK activation and the epithelial barrier function impairment of IPEC-J2. Furthermore, inhibition of MLCK totally abolished the impairment of epithelial barrier function induced by c9, t11-CLA. In vivo, dietary supplementation of c9, t11-CLA rather than t10, c12-CLA isomer decreased the expression of intestinal tight junction proteins and GPR120, increased intestinal permeability, and activated the MLCK signaling pathway in mice. Taken together, our findings showed that c9, t11-CLA, but not t10, c12-CLA isomer, impaired intestinal epithelial barrier function in IPEC-J2 cells and mice through activation of GPR120-[Ca2+]i and the MLCK signaling pathway. These data provided new insight into the regulation of the intestinal epithelial barrier by different CLA isomers and more references for CLA application in humans and animals.

Bile acids (BAs) have been implicated in regulation of intestinal epithelial signaling and function. This study aimed to investigate the effects of hyodeoxycholic acid (HDCA) on intestinal epithelial cell proliferation and explore the underlying mechanisms. IPEC-J2 cells and weaned piglets were treated with HDCA and the contributions of cellular signaling pathways, BAs metabolism profiles and gut bacteria were assessed. In vitro, HDCA suppressed IPEC-J2 proliferation via the BAs receptor FXR but not TGR5. In addition, HDCA inhibited the PI3K/AKT pathway, while knockdown of FXR or constitutive activation of AKT eliminated the inhibitory effects of HDCA, suggesting that FXR-dependent inhibition of PI3K/AKT pathway was involved in HDCA-suppressed IPEC-J2 proliferation. In vivo, dietary HDCA inhibited intestinal expression of proliferative markers and PI3K/AKT pathway in weaned piglets. Meanwhile, HDCA altered the BAs metabolism profiles, with decrease in primary BA and increase in total and secondary BAs in feces, and reduction of conjugated BAs in serum. Furthermore, HDCA increased abundance of the gut bacteria associated with BAs metabolism, and thereby induced BAs profiles alternation, which might indirectly contribute to HDCA-suppressed cell proliferation. Together, HDCA suppressed intestinal epithelial cell proliferation through FXR-PI3K/AKT signaling pathway, accompanied by alteration of BAs metabolism profiles induced by gut bacteria.

[目的]研究日粮添加鱼油对高脂日粮饲喂小鼠肠道屏障功能的影响.[方法]选用36只4周龄C57BL/6J雌性小鼠,随机分为对照组、高脂组、高脂+鱼油组,每组12只小鼠,分别饲喂基础日粮、高脂日粮、高脂日粮添加质量分数为5％的鱼油(等能替换高脂日粮中脂肪).试验持续21周,每周测定小鼠采食量和体质量,期间测定小鼠肠道通透性以及粪便粗脂肪含量和能值;试验结束后,检测小鼠血清内毒素水平,检测小鼠肠道形态、杯状细胞的数量、肠道紧密连接蛋白和炎症因子的表达.[结果]与高脂组相比,日粮添加鱼油显著提高了小鼠采食量和能量摄入、降低了粪便中粗脂肪的含量和能量排出,显著降低了小鼠体质量(P<0.05).在肠道形态方面,与高脂组相比,添加鱼油使小鼠空肠和回肠的绒毛高度与隐窝深度比值(lV/dC)分别提高了43.1％和67.5％,使回肠绒毛杯状细胞的数量增多了16.7％(P<0.05).与高脂组相比,添加鱼油使血清荧光葡聚糖和内毒素水平分别降低了34.3％和50.4％(P<0.05),并逆转了高脂日粮造成的肠道紧密连接蛋白表达的降低.在炎症因子表达方面,与高脂组相比,添加鱼油显著降低了空肠和回肠内促炎因子IL-8、IL-6和IL-1β的表达,同时显著增加了抗炎因子IL-10的表达(P<0.05).[结论]日粮添加鱼油可降低由高脂日粮导致的小鼠肠道屏障功能损伤,这可能与鱼油降低肠道炎症有关.

This study aimed to investigate the effects of Actigen (TM), a second-generation mannan rich fraction, on growth performance, intestinal morphology and permeability, and intestinal inflammatory response in weaned piglets. A total of 150 healthy weaned piglets were randomly assigned to the Control, Antibiotics and Actigen groups and received 1 of 3 dietary treatments: a basal antibiotics-free diet to which 250 mg/kg antibiotics (100 mg/kg colistin sulfate, 100 mg/kg olaquindox, and 50 mg/kg Kitasamycin) or 800 mg/kg Actigen were added. Body weight and feed intake were recorded. On day 28 of experimentation, five female and five male piglets per treatment were selected to collect blood, small intestinal segments and mucosa samples. Intestinal morphology and goblet cell number were determined. Expression of tight junction proteins and TLR4 signaling were detected. n-lactic acid (DLA) and inflammatory cytokines in serum were also measured. Compared with the Control group, Actigen and antibiotics supplemented diets reduced incidence of diarrhea (P < 0.05), with no effect on growth performance. Intestinal morphology revealed that antibiotics decreased (P < 0.01), while Actigen increased the villus height and the ratio of villus height to crypt depth (P < 0.01). PAS staining demonstrated that the goblet cell, number was elevated in jejunum of the Actigen fed piglets compared with the Antibiotics group (P < 0.05). In addition, the use of antibiotics decreased the expression of tight junction proteins (P < 0.05), while the use of Actigen increased it (P < 0.05). Accordingly, the intestinal permeability was elevated by antibiotics use, with the increased serum DLA (P < 0.05). Furthermore, Actigen fed piglets had lower serum proinflammatory cytokine TNF-alpha (P < 0.05) and higher serum anti-inflammatory cytokine IL-10 (P < 0.05). In contrast, antibiotics use led to an increase of serum IL-1 beta (P < 0.05). Moreover, the expression of TLR4, Myd88, and IKK beta phosphyorlation were enhanced by antibiotics use (P < 0.05), suggesting the activation of TLR4 signaling pathway. However, Actigen supplemented diet had no effect on the TLR4 signaling pathway. In conclusion, compared with the Control group, Actigen supplemented diet had no effects on ADG, ADFI and FCR, but reduced the incidence of diarrhea and mortality to the similar level as the Antibiotics group. Actigen also improved the intestinal morphology and permeability, reduced intestinal inflammatory response compared with the Antibiotics group. These findings suggested the potential application of Actigen in weaned piglets production.

This study aimed to investigate the effects of ActigenTM, a second-generation mannan rich fraction, on growth performance, intestinal barrier functions and inflammation in weaned piglets. A total of 150 weaned piglets were randomly assigned to Control, antibiotics and Actigen groups and received 1 of 3 dietary treatments: a basal antibiotics-free diet to which 100 mg/kg antibiotics or 800 mg/kg Actigen were added. Body weight and feed intake were recorded. On day 28, 10 piglets per treatment were selected to collect blood, small intestinal segments and mucosa samples. Intestinal morphology and goblet cell number were determined. Expression of tight junction proteins and Toll Like receptor 4 (TLR4) signaling were detected. D-lactic acid (DLA) and inflammatory cytokines in serum were also measured. Actigen or antibiotics supplemented diets significantly reduced incidence of diarrhea, with no effect on growth performance. Intestinal morphology revealed that antibiotics significantly decreased, while Actigen markedly increased the villus height and the ratio of villus height to crypt depth. PAS staining demonstrated that the goblet cell number was markedly elevated in jejunum of the Actigen fed piglets. In addition, the expression of tight junction proteins was significantly decreased and increased by antibiotics and Actigen use, respectively. Accordingly, the intestinal permeability was elevated by antibiotics use, with the increased serum DLA. Furthermore, Actigen fed piglets had lower serum proinflammatory cytokine TNF-α and higher serum anti-inflammatory cytokine IL-10. In contrast, antibiotics use led to the increase of serum IL-1β. Moreover, the expression of TLR4, Myd88, and IKKβ phosphyorlation were enhanced by antibiotics use, suggesting the activation of TLR4 signaling pathway. However, Actigen supplemented diet had no effect on the TLR4 signaling pathway. In conclusion, compared with the control and antibiotics groups, Actigen supplemented diet had the similar or improved effects on growth performance, intestinal barrier functions and inflammation in weaned piglets.

[目的]研究饮水添加氯化钙对高脂日粮饲喂小鼠脂肪沉积和肠道菌群的影响,为提高动物胴体品质和人体健康提供理论依据.[方法]选用27只4周龄C57BL雄性小鼠,分为高脂日粮组和高脂日粮+饮水添加氯化钙组,试验期13周.每周测定小鼠体质量,试验末测定小鼠体脂含量,试验结束后采集小鼠皮下脂肪、附睾脂肪并称质量.于试验后期10～12周采集小鼠粪便进行16S rRNA高通量测序,并分析对菌群的影响.[结果]饮水添加氯化钙显著降低了小鼠体质量、体脂含量、皮下脂肪指数和附睾脂肪指数,与高脂组相比分别降低了12.85％、32.69％、26.65％和18.60％.饮水添加氯化钙提高了小鼠粪便样中的菌群多样性和菌群丰度.在门水平下,饮水添加氯化钙对拟杆菌门Bacteroidetes、厚壁菌门Firmicutes、变形菌门Proteobacteria、脱铁杆菌门Deferribacteres、放线菌门Actinobacteria、软壁菌门Tenericutes的丰度无明显影响.在纲水平下,与高脂组相比,饮水添加氯化钙显著降低了丹毒丝菌纲Erysipelotrichia和放线菌纲Actinobacteria的相对丰度,并且显著提高了梭菌纲Clostridia的相对丰度.[结论]饮水添加氯化钙能够降低高脂日粮饲喂小鼠的体质量和体脂含量,这可能与饮水添加氯化钙提高了小鼠粪便菌群多样性和特定菌群丰度有关.

Obesity has been demonstrated as a disruptor of female fertility. Our previous study showed the antiobesity effects of calcium on HFD-fed male mice. However, the role of calcium in alleviating reproductive dysfunction of HFD-fed female mice remains unclear. Here, we found that HFD led to estrus cycle irregularity (longer cycle duration and shorter estrus period) and subfertility (longer conception time, lower fertility index, and less implantations) in mice. However, the HFD-induced reproductive abnormality was alleviated by calcium supplementation. Additionally, calcium supplementation enhanced activation/thermogenesis of BAT and browning of WAT in HFD-fed mice. Consequently, the abnormality of energy metabolism and glucose homeostasis induced by HFD were improved by calcium supplementation, with elevated metabolic rates and core temperature. In conclusion, these data showed that calcium supplementation alleviated HFD-induced estrous cycle irregularity and subfertility associated with concomitantly enhanced BAT thermogenesis and WAT browning, suggesting the potential application of calcium in improving obesity-related reproductive disorders.

The development of muscle in the embryo, which is crucial for postnatal skeletal muscle growth, has been investigated widely. Much has been learned during the past several decades about the role of maternal nutrition in the outcome of pregnancy. Protein and carbohydrate levels during pregnancy have been shown to be important in the development of offspring, especially muscle development. However, the maternal effects of steroids were still not clear. Phytosterol esters (PEs) are produced by the esterification of phytosterols and fatty acids and have many beneficial functions, such as anti-inflammation and hypolipemic functions. Through the effect of regulation on lipid metabolism, can pregnant mice fed with PEs show any programming effect on the muscle development of offspring? In our study, PEs were supplied to the maternal diet, and changes in maternal lipid metabolism and the development of offspring skeletal muscle were detected. As a result, the amniotic fluid total bile acid (TBA) and total cholesterol (TC) levels were decreased; the growth of offspring was significantly faster than that of the control group until 6 weeks of age. Adult offspring had a higher lean mass index and grip strength. In skeletal muscle, the proportion of myosin heavy chain (MHC) 1 was significantly decreased, while the proportion of MHC 2 b was increased. In conclusion, maternal PEs significantly reduced sterols in the amniotic fluid, while skeletal muscle development was promoted in the offspring.

Chenodeoxycholic acid (CDCA), a primary bile acid, has been demonstrated to play important roles as a signaling molecule in various physiology functions. However, the role of CDCA in regulating intestinal barrier function remains largely unknown. This study aimed to investigate the effects of CDCA on the lipopolysaccharide (LPS)-impaired intestinal epithelial barrier function and explore the underlying mechanisms. In IPEC-J2 cells, CDCA reversed the LPS-induced increase in transepithelial electrical resistance and decrease in tight junction protein expression. In addition, we found that farnesoid X receptor (FXR) but not Takeda G-protein receptor 5 was responsible for the CDCA-improved epithelial barrier function impaired by LPS. Furthermore, CDCA blocked LPS-induced activation of the myosin light chain kinase (MLCK) pathway in a FXR-dependent manner and elicited similar effects to MLCK inhibition. In mice, CDCA supplementation restored LPS-induced elevation of intestinal permeability and MLCK expression and reduction of tight junction protein expression, thus alleviating LPS-induced intestinal barrier impairment. In conclusion, CDCA protected against the LPS-induced impairment of the intestinal epithelial barrier function via the FXR-MLCK pathway.

BACKGROUND/AIMS:It has been implicated that calcium supplementation is involved in reducing body weight/fat and improving glucose homeostasis. However, the underlying mechanisms are still not fully understood. Here, we investigated the effects of calcium supplementation on adipogenesis and glucose homeostasis in porcine bone marrow mesenchymal stem cells (pBMSCs) and high fat diet (HFD)-fed mice and explored the involved signaling pathways.METHODS:In vitro, pBMSCs were treated with 4 mM extracellular calcium ([Ca2+]o) and/or 1 μM nifedipine, 0.1 μM BAPTA-AM, 1 μM KN-93, 50 nM wortmannin for 10 days. The intracellular calcium ([Ca2+]i) levels were measured using Fluo 3-AM by flow cytometry. The adipogenic differentiation of pBMSCs was determined by Oil Red-O staining and triglyceride assay. The expression of marker genes involved in adipogenesis (peroxisome proliferator activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα)) and glucose uptake (glucose transporter 4 (GLUT4)), as well as the activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and PI3K/Akt-FoxO1/AS160 signaling pathways were determined by Western blotting. Glucose uptake and utilization were examined using 2-NBDG assay and glucose content assay, respectively. In vivo, C57BL/6J male mice were fed a HFD (containing 1.2% calcium) without or with 0.6% (w/w) calcium chloride in drinking water for 13 weeks. The adipogenesis, glucose homeostasis and the involvement of CaMKII and PI3K/Akt signaling pathway were also assessed.RESULTS:In vitro, [Ca2+]o stimulated pBMSCs adipogenesis by increasing [Ca2+]i level and activating CaMKII and PI3K/Akt-FoxO1 pathways. In addition, [Ca2+]o promoted glucose uptake/utilization by enhancing AS160 phosphorylation, GLUT4 expression and translocation. However, the stimulating effects of [Ca2+]o on pBMSCs adipogenesis and glucose uptake/utilization were abolished by L-VGCC blocker Nifedipine, [Ca2+]i chelator BAPTA-AM, CaMKII inhibitor KN-93, or PI3K inhibitor Wortmannin. In vivo, calcium supplementation decreased body weight and fat content, increased adipocyte number, and improved glucose homeostasis, with elevated PPARγ and GLUT4 expression and PI3K/Akt activation in iWAT.CONCLUSION:calcium supplementation enhanced adipogenesis and glucose uptake in pBMSCs, which was coincident with the increased adipocyte number and improved glucose homeostasis in HFD-fed mice, and was associated with activation of CaMKII and PI3K/Akt-FoxO1/AS160 pathways. These data provided a broader understanding of the mechanisms underlying calcium-induced body weight/fat loss and glycemic control.

This study aimed to investigate the effects of oleic acid (OA), a monounsaturated fatty acid, on HC11 mammary epithelial cells proliferation and peripubertal mammary gland development and explore the underlying mechanisms. HC11 cells and C57BL/6J mice were treated with OA. HC11 proliferation, peripubertal mammary gland development, and the involvement of CD36 and PI3K/Akt were assessed. In vitro, 100 μM OA significantly promoted HC11 proliferation by increasing Cyclin D1/3 and PCNA expression and decreasing p21 expression. Meanwhile, OA enhanced CD36 expression, elevated [Ca2+]i and activated PI3K/Akt signaling pathway. However, knockdown of CD36, chelation of [Ca2+]i or inhibition of PI3K eliminated the OA-induced promotion of HC11 proliferation and change in proliferative markers expression. In vivo, peripubertal exposure to diet containing 2% OA stimulated mammary duct development, with increased terminal duct end (TDE) and ductal branch. Moreover, dietary OA increased the serum levels of IGF-1 and E2, enhanced the expression of CD36 and Cyclin D1, and activated PI3K/Akt pathway in mammary glands. In conclusion, OA stimulated HC11 cells proliferation and mammary gland development in peripubertal mice, which was associated with activation of CD36-[Ca2+]i and PI3K/Akt signaling pathway. These data provided new insights into the stimulation of mammary gland development by dietary oleic acid.

Stimulating the browning of white adipocytes contributes to the restriction of obesity and related metabolic disorders. This study aimed to investigate the browning effects of phytol on mice inguinal subcutaneous white adipose tissue (iWAT) and explore the underlying mechanisms. Our results demonstrated that phytol administration decreased body weight gain and iWAT index, and stimulated the browning of mice iWAT, with the increased expression of brown adipocyte marker genes (UCP1, PRDM16, PGC1α, PDH, and Cyto C). In addition, phytol treatment activated the AMPKα signaling pathway in mice iWAT. In good agreement with the in vivo findings, the in vitro results showed that 100 μM phytol stimulated brown adipogenic differentiation and formation of brown-like adipocytes in the differentiated 3T3-L1 by increasing the mitochondria content and oxygen consumption, and promoting mRNA and/or protein expression of brown adipocyte markers (UCP1, PRDM16, PGC1α, PDH, Cyto C, Cidea and Elovl3) and beige adipocyte markers (CD137 and TMEM26). Meanwhile, phytol activated the AMPKα signaling pathway in the differentiated 3T3-L1. However, the inhibition of AMPKα with Compound C totally abolished phytol-stimulated brown adipogenic differentiation and formation of brown-like adipocytes. In conclusion, these results showed that phytol stimulated the browning of mice iWAT, which was coincident with the increased formation of brown-like adipocytes in the differentiated 3T3-L1, and appeared to be primarily mediated by the AMPKα signaling pathway. These data provided new insight into the role of phytol in regulating the browning of WAT and suggested the potential application of phytol as a nutritional intervention for the restriction of obesity and related metabolic disorders.

The effects of four phytotoxins usnic acid (UA), salicylic acid (SA), cinnamic acid (CA) and benzoic acid (BA) on photosynthesis of Chlamydomonas reinhardtii were studied in vivo to identify and localise their initial action sites on two photosystems. Our experimental evidence shows that the four phytotoxins have multiple targets in chloroplasts, which mainly lie in photosystem II (PSII), not photosystem I (PSI). They share an original action site by blocking electron transport beyond QA (primary plastoquinone acceptor) at PSII acceptor side since a fast increase of the J-step level is the greatest change in chlorophyll a fluorescence induction kinetics OJIP in C. reinhardtii cells treated with the phytotoxins. UA decreases photosynthetic activity by reducing O2 evolution rate, interrupting PSII electron transport at both the donor and acceptor sides, inactivating the PSII reaction centers (RCs), reducing the content of chlorophylls and carotenoids, destroying the conformation of antenna pigment assemblies, and casuing the degradation of D1/D2 proteins. SA damage to photosynthetic machinery is mainly attributed to inhibition of PSII electron transport beyond QA at the acceptor side, inactivation of the PSII RCs, reduction of chlorophyll content, digestion of thylakoid ploypeptides and destabilization of thylakoid membranes. Both CA and BA affect the photosynthetic process by decreasing PSII electron transport efficiency at the acceptor side and the amount of active PSII RCs. Besides, the initial cause of BA-inhibiting photosynthesis is also assocaited with the O2 evolution rate and the disconnection of some antenna molecules from PSII RCs.