Targeting serum response factor (SRF) deactivates ΔFosB and mitigates Levodopa-induced dyskinesia in a mouse model of Parkinson's disease.

L-3,4-dihydroxyphenylalanine (L-DOPA) is currently the preferred treatment for Parkinson's Disease (PD) and is considered the gold standard. However, prolonged use of L-DOPA in patients can result in involuntary movements known as Levodopa-induced dyskinesia (LID), which includes uncontrollable dystonia affecting the trunk, limbs, and face. The role of ΔFosB protein, a truncated splice variant of the FosB gene, in LID has been acknowledged, but its underlying mechanism has remained elusive. Here, using a mouse model of Parkinson's disease treated with chronic levodopa we demonstrate that serum response factor (SRF) binds to the FosB promoter, thereby activating FosB expression and levodopa induced-dyskinetic movements. Western blot analysis demonstrates a significant increase in SRF expression in the dyskinetic group compared to the control group. Knocking down SRF significantly reduced abnormal involuntary movements (AIMS) and ΔFosB expression compared to the control. Conversely, overexpression of SRF led to an increase in ΔFosB expression and worsened levodopa-induced dyskinesia. To shed light on the regulatory role of the Akt signaling pathway in this phenomenon, we administered the Akt agonist SC79 to PD mouse models via intraperitoneal injection, followed by L-DOPA administration. The expression of SRF, ΔFosB, and phosphorylated Akt (p-Akt) significantly increased in this group compared to the group receiving normal saline to signify that these happen through Akt signaling pathway. Collectively, our findings identify a promising therapeutic target for addressing levodopa-induced dyskinesia.

CXCR4-overexpressed exosomes from cardiosphere-derived cells attenuate myocardial ischemia/reperfusion injury by transferring miRNA to macrophages and regulating macrophage polarization.

Cardiosphere-derived cells (CDCs) are emerging as ideal candidates for managing cardiac inflammation, albeit with some limitations. Recent literatures have indicated that exosomes secreted by CDCs with C-X-C motif chemokine receptor 4 (CXCR4) overexpression can promote cardiac function after myocardial infarction and there have been some reports of miRNAs involved in ischemia/reperfusion (I/R) therapy. Therefore, we are interested in the role of CXCR4-overexpressed CDC-derived exosomes in delivering specific miRNA after myocardial I/R injury. In this research, we first constructed CDC-derived exosomes that overexpressed CXCR4 and miR-27a-5p, miR-182, or miR-101a. Then, we co-cultured the engineered exosomes with RAW264.7 cells and injected them intravenously into myocardial I/R model mice. In vitro, results showed that proinflammatory cytokines levels in the culture supernatant were decreased and the expression of M2 phenotypic markers were increased. Administration of engineered exosomes improved cardiac function, reduced infarct size, alleviated macrophage infiltration, and regulated M2 macrophage polarization after myocardial I/R, suggesting their implications in cardiac injury repair.

Mechanism of TiO2 nanoparticle-induced neurotoxicity in zebrafish (Danio rerio).

Zebrafish (Danio rerio) has been used historically for evaluating the toxicity of environmental and aqueous toxicants, and there is an emerging literature reporting toxic effects of manufactured nanoparticles (NPs) in zebrafish embryos. Few researches, however, are focused on the neurotoxicity on adult zebrafish after subchronic exposure to TiO2 NPs. This study was designed to evaluate the morphological changes, alterations of neurochemical contents, and expressions of memory behavior-related genes in zebrafish brains caused by exposures to 5, 10, 20, and 40 µg/L TiO2 NPs for 45 consecutive days. Our data indicated that spatial recognition memory and levels of norepinephrine, dopamine, and 5-hydroxytryptamine were significantly decreased and NO levels were markedly elevated, and over proliferation of glial cells, neuron apoptosis, and TiO2 NP aggregation were observed after low dose exposures of TiO2 NPs. Furthermore, the low dose exposures of TiO2 NPs significantly activated expressions of C-fos, C-jun, and BDNF genes, and suppressed expressions of p38, NGF, CREB, NR1, NR2ab, and GluR2 genes. These findings imply that low dose exposures of TiO2 NPs may result in the brain damages in zebrafish, provide a developmental basis for evaluating the neurotoxicity of subchronic exposure, and raise the caution of aquatic application of TiO2 NPs.

TiO2 nanoparticle-induced neurotoxicity may be involved in dysfunction of glutamate metabolism and its receptor expression in mice.

Titanium dioxide nanoparticles (TiO2 NPs) have been used in environmental management, food, medicine, and industry. But TiO2 NPs have been demonstrated to cross the blood-brain barrier and store up in the brain organization, leading to glutamate-mediated neurotoxicity. However, the neurotoxicity in the brain is not well understood. In this study, mice were exposed to 1.25, 2.5, or 5 mg/kg body weight TiO2 NPs for 9 months, and the glutamate-glutamine cyclic pathway and expressions of glutamate receptors associated with the hippocampal neurotoxicity were investigated. Our findings showed elevations of glutamate release and phosphate-activated glutaminase activity, and reductions in glutamine and glutamine synthetase in the hippocampus following exposure to TiO2 NPs. Furthermore, TiO2 NPs significantly inhibited the expression of N-methyl-d-aspartate receptor subunits (including NR1, NR2A, and NR2B) and metabotropic glutamate receptor 2 in mouse hippocampus. These findings suggest that the imbalance of glutamate metabolism triggered inhibitions of glutamate receptor expression in the TiO2 NP-exposed hippocampus. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 655-662, 2016.

Nanoparticulate TiO2 protection of midgut damage in the silkworm (Bombyx mori) following phoxim exposure.

Bombyx mori (B. mori) is often subjected to phoxim poisoning in China due to phoxim exposure, which leads to a decrease in silk production. Nanoparticulate (NP) titanium dioxide (nano-TiO2) has been shown to attenuate damages in B. mori caused by phoxim exposure. However, little is known about the molecular mechanisms of midgut injury due to organophosphorus insecticide exposure and its repair by nano-TiO2 pretreatment. In this study, phoxim exposure for 36 h led to significant decreases in body weight and survival and increased oxidative stress and midgut injury. Pretreatment with nano-TiO2 attenuated the phoxim-induced midgut injury, increased body weight and survival, and decreased oxidative stress in the midgut of B. mori. Digital gene-expression data showed that exposure to phoxim results in significant changes in the expression of 254 genes in the phoxim-exposed midgut and 303 genes in phoxim + nano-TiO2-exposed midgut. Specifically, phoxim exposure led to upregulation of Tpx, α-amylase, trypsin, and glycoside hydrolase genes involved in digestion and absorption. Phoxim exposure also led to the downregulation of Cyp450 and Cyp4C1 genes involved in an antioxidant capacity. In contrast, a combination of both phoxim and nano-TiO2 treatment significantly decreased the change in α-amylase, trypsin, and glycoside hydrolases (GHs), which are involved in digestion and absorption. These results indicated that Tpx, α-amylase, trypsin, GHs, Cyp450, and Cyp4C1 may be potential biomarkers of midgut toxicity caused by phoxim exposure and the attenuation of these toxic impacts by nano-TiO2.

High expression of COPZ2 is associated with poor prognosis and cancer progression in glioma.

Background: Coatomer protein complex zeta 2 (COPZ2) is a member of heptameric coatomer protein complex I and has been reported to be involved in various tumors. However, COPZ2's potential involvement in glioma remains to be explored. Methods: The COPZ2 expression and related clinical data were obtained from The Cancer Genome Atlas (TCGA). TIMER2.0 and the Ualcan database were utilized to assess the COPZ2 expression in various tumors. Univariable, multivariate Cox regression, Kaplan-Meier methods, nomogram analysis, and ROC curve analysis were carried out to assess the relationship of COPZ2 and other prognostic factors with glioma. The LinkedOmics database was used to predict the potential biological mechanism of COPZ2 in glioma. We also conducted in vitro experiments to evaluate the functional role and mechanism of COPZ2 in glioma cell lines. Results: We found that COPZ2 was highly expressed in glioma and it was associated with age and WHO grades. Kaplan-Meier survival curves, Cox analysis, nomogram analysis, and ROC curve showed that COPZ2 was a disadvantageous factor in poor glioma prognosis. The functions of COPZ2 and co-expression genes were significantly associated with neutrophil-mediated immunity, granulocyte activation, and response to interferon-gamma. In addition, COPZ2 knockdown significantly inhibited the proliferation, migration, and invasion of glioblastoma cells. Mechanistically, COPZ2 suppressed tumor development by participating in the regulation of the PI3K-AKT signaling pathway. Conclusion: Our results demonstrated that the elevation of COPZ2 was associated with the prognosis and progression of glioma, and it might be a potential diagnostic and prognostic biomarker for glioma.

The Aggregation of α-Synuclein in the Dorsomedial Striatum Significantly Impairs Cognitive Flexibility in Parkinson's Disease Mice.

This study focused on α-synuclein (α-syn) aggregation in the dorsomedial striatum (DMS) so as to investigate its role in the cognitive flexibility of Parkinson's disease (PD). Here, we investigated the cognitive flexibility by assessing reversal learning abilities in MPTP-induced subacute PD model mice and in C57BL/6J mice with α-syn aggregation in the DMS induced by adenovirus (AAV-SNCA) injection, followed by an analysis of the target protein's expression and distribution. PD mice exhibited impairments in reversal learning, positively correlated with the expression of phosphorylated α-syn in the DMS. Furthermore, the mice in the AAV-SNCA group exhibited reversal learning deficits and a reduction in acetylcholine levels, accompanied by protein alterations within the DMS. Notably, the administration of a muscarinic receptor 1 (M1R) agonist was able to alleviate the aforementioned phenomenon. These findings suggest that the impaired cognitive flexibility in PD may be attributed to the diminished activation of acetylcholine to M1R caused by α-syn aggregation.

Serum miR-497-5p serves as a diagnostic biomarker for acute coronary syndrome and predicts the occurrence of major adverse cardiovascular events after percutaneous coronary intervention.

This study aimed to investigate the diagnostic value of microRNA (miR)-497-5p in acute coronary syndrome (ACS) and its predictive value for the occurrence of adverse major adverse cardiovascular events (MACEs). Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to detect the expression of serum miR-497-5p in 110 ACS patients and 82 controls. And miR-497-5p levels were found to be significantly elevated in the patients (P < 0.001). Pearson correlation coefficient confirmed that miR-497-5p was positively correlated with Gensini scores (r = 0.684). The area under the Receiver-operating characteristic (ROC) curve was 0.861, which significantly identified patients with ACS, and was confirmed by logistic regression (OR = 8.533, 95%CI = 4.113-17.787, P < 0.001). Kaplan-Meier and Cox regression was performed to evaluate the predictive value of miR-497-5p in the occurrence of MACEs during a 6-month follow-up after percutaneous coronary intervention (PCI) in patients with ACS. The results demonstrated that miR-497-5p was an independent predictor of MACEs (HR = 4.773, 95%CI = 1.569-12.036, P = 0.013) and that patients with high level of miR-497-5p were more likely to develop MACEs after PCI (long-rank P = 0.019). Finally, miR-497-5p positively correlated with endothelial proinflammatory and adhesion factors. Our study suggests that serum miR-497-5p is a potential diagnostic marker for ACS and its elevated levels can predict a high risk of MACEs in ACS patients after PCI. And this may be associated with vascular endothelial injury.

Novel insights into impacts of the COVID-19 pandemic on aquatic environment of Beijing-Hangzhou Grand Canal in southern Jiangsu region.

In 2020, a sudden COVID-19 pandemic unprecedentedly weakened anthropogenic activities and as results minified the pollution discharge to aquatic environment. In this study, the impacts of the COVID-19 pandemic on aquatic environment of the southern Jiangsu (SJ) segment of Beijing-Hangzhou Grand Canal (SJ-BHGC) were explored. Fluorescent component similarity and high-performance size exclusion chromatography analyses indicated that the textile printing and dyeing wastewater might be one of the main pollution sources in SJ-BHGC. The water quality parameters and intensities of fluorescent components (WT-C1(20) and WT-C2(20)) decreased to low level due to the collective shutdown of all industries in SJ region during the Spring Festival holiday and the outbreak of the domestic COVID-19 pandemic in China (January 24th to late February, 2020). Then, they presented a gradual upward trend after the domestic epidemic was under control. In mid-March, the outbreak of the international COVID-19 pandemic hit the garment export trade of China and consequently inhibited the production activities of textile printing and dyeing industry (TPDI) in SJ region. After peaking on March 26th, the intensities of WT-C1(20) and WT-C2(20) decreased again with changed intensity ratio until April 12th. During the study period (135 days), correlation analysis revealed that WT-C1 and WT-C2 possessed homology and their fluorescence intensities were highly positively correlated with conductivity and CODMn. With fluorescence fingerprint (FF) technique, this study not only excavated the characteristics and pollution causes of water body in SJ-BHGC, but also provided novel insights into impacts of the COVID-19 pandemic on production activities of TPDI and aquatic environment of SJ-BHGC. The results of this study indicated that FF technique was an effective tool for precise supervision of water environment.

Promotion of nano-anatase TiO(2) on the spectral responses and photochemical activities of D1/D2/Cyt b559 complex of spinach.

Previous researches approved that photocatalysis activity of nano-TiO(2) could obviously increase photosynthetic effects of spinach, but the mechanism of improving light energy transfer and conversion is still unclear. In the present we investigated effects of nano-anatase TiO(2) on the spectral responses and photochemical activities of D1/D2/Cyt b559 complex of spinach. Several effects of nano-anatase TiO(2) were observed: (1) UV-vis spectrum was blue shifted in both Soret and Q bands, and the absorption intensity was obviously increased; (2) resonance Raman spectrum showed four main peaks, which are ascribed to carotene, and the Raman peak intensity was as 6.98 times as that of the control; (3) the fluorescence emission peak was blue shifted and the intensity was decreased by 23.59%; (4) the DCPIP photoreduction activity showed 129.24% enhancement; (5) the oxygen-evolving rate of PS II was elevated by 51.89%. Taken together, the studies of the experiments showed that nano-anatase TiO(2) had bound to D1/D2/Cyt b559 complex, promoted the spectral responses, leading to the improvement of primary electron separation, electron transfer and light energy conversion of D1/D2/Cyt b559 complex.

Increased serum bile acid level is associated with high-risk coronary artery plaques in an asymptomatic population detected by coronary computed tomography angiography.

BACKGROUND: There are limited data on the association between serum total bile acid level and coronary plaque characteristics. This study investigated the relationship between serum total bile acid level and the severity of coronary stenosis and coronary plaque features in an asymptomatic population using coronary computed tomography angiography (CTA). METHODS: A total of 1,137 consecutive participants with no known coronary artery disease (CAD) undergoing CTA as part of a general routine health evaluation were recruited. Serum total bile acid level and clinical parameters were assayed. Coronary stenosis and high-risk plaques features (napkin-ring sign, low-attenuation plaque, spotty calcification, positive remodelling) were evaluated. Associations between serum total bile acid concentration and high-risk coronary plaques was tested through univariate and multivariate analyses. RESULTS: A total of 101 high-risk coronary plaques subjects and 93 controls were eligible for study inclusion. The severity of coronary artery stenosis and high-risk coronary plaques increased with serum total bile acid level quartiles (all P<0.001). The independent predictor of high-risk coronary plaques in multivariate analysis was serum total bile acid level (P<0.001). Receiver operating characteristic (ROC) confirmed that serum total bile acid concentration significantly differentiated high-risk coronary plaques [the area under the curve (AUC) =0.876; P<0.001, with a sensitivity of 87.13% and a specificity of 86.02%]. CONCLUSIONS: Higher serum total bile acid level was associated with the severity of coronary artery stenosis and high-risk coronary artery plaques detected by CTA in asymptomatic populations.

Effects of nanoanatase on the photosynthetic improvement of chloroplast damaged by linolenic acid.

To further evaluate the photosynthetic effects of nanoanatase, the improvement of spinach chloroplast photosynthesis damaged by linolenic acid was investigated in the present paper. Several results showed that after the addition of nanoanatase to the linolenic acid-treated chloroplast, the light absorption increased by linolenic acid could be decreased, but the excitation energy distribution from photosystem (PS) I to PS II was promoted, and the decrease of PS II fluorescence yield caused by linolenic acid was reduced and the inhibition of oxygen evolution caused by linolenic acid of several concentrations was decreased. It was considered that nanoanatase could combine with linolenic acid and decrease the damage of linolenic acid on the structure and function of chloroplast.

Influences of lead (II) chloride on the nitrogen metabolism of spinach.

Lead (Pb(2+)) is a well-known highly toxic element. The mechanisms of the Pb(2+) toxicity are not well understood for nitrogen metabolism of higher plants. In this paper, we studied the effects of various concentrations of PbCl(2) on the nitrogen metabolism of growing spinach. The experimental results showed that Pb(2+) treatments significantly decreased the nitrate nitrogen (NO(-)(3)-N) absorption and inhibited the activities of nitrate reductase, glutamate dehydrogenase, glutamine synthase, and glutamic-pyruvic transaminase of spinach, and inhibited the synthesis of organic nitrogen compounds such as protein and chlorophyll. However, Pb(2+) treatments increased the accumulation of ammonium nitrogen NH(+)(4)-N)in spinach cell. It implied that Pb(2+) could inhibit inorganic nitrogen to be translated into organic nitrogen in spinach, thus led to the reduction in spinach growth.

Nano-anatase relieves the inhibition of electron transport caused by linolenic acid in chloroplasts of spinach.

Linolenic acid is an inhibitor of electron transport in chloroplasts of higher plants. It has obvious effects on the structure and function of chloroplasts. In the present paper, we investigated the nano-anatase relieving the inhibition of photoreduction activity and oxygen evolution caused by linolenic acid in spinach chloroplasts. The results showed that linolenic acid in various concentrations could obviously reduce the whole chain electron transport and the photoreduction activity of two photosystems, especially on the oxidative reside and reduce reside of photosystem II (PS II). After adding nano-anatase to chloroplasts treated by linolenic acid, the whole chain electron transport rate, the photoreduction activity of two photosystems, and the oxygen evolution rate were increased significantly, indicating that nano-anatase could obviously decrease the inhibition of linolenic acid on the electron transport, photoreduction activity, and oxygen evolution of spinach chloroplasts.

Effects of Pb2+ on energy distribution and photochemical activity of spinach chloroplast.

Lead (Pb(2+)) is a well-known highly toxic element. The mechanisms of the Pb(2+) toxicity are not well understood for photosynthesis. In this paper, we reported the effect of Pb(2+) on light absorption, distribution and conversion of spinach chloroplast by spectroscopy, and photochemical reaction activities. Several effects of Pb(2+) were observed: (1) the absorption peak intensity of chloroplast obviously decreased in red and blue region and produced optical flattering; (2) fluorescence quantum yield nearby 680 nm of chloroplast greatly declined; (3) the excitation band nearby 440 nm of chloroplast significantly descended; (4) Pb(2+) treatments reduced of the rate of whole chain electron transport, photochemical activities of PSII DCPIP photoreduction and oxygen evolution, but the photoreduction activities of PSI were little changed. Together, the studies of the experiments showed that Pb(2+) decreased absorption of light on spinach chloroplast and inhibited excitation energy to be absorbed by LHCII and transferred to PSII, then reduced the conversion from light energy to electron energy, and decelerated electron transport, water photolysis and oxygen evolution.

Mechanism of Cd2+ on DNA cleavage and Ca2+ on DNA repair in liver of silver crucian carp.

The subject of acute injury, apoptosis and canceration of animals induced by heavy metal ions has been one of the hotspots studied worldwide. However, the exact molecular mechanism of Cd-induced carcinogenicity remains largely unclear, and how to relieve the toxicity in vivo has rarely been reported. For this paper, we have investigated the mechanism of Cd2+ on DNA cleavage and Ca2+ on DNA repair in the liver of silver crucian carp (Carassius auratus gibelio) by agarose gel electrophoresis methods and by estimating biochemical indexes. Our results show that Cd2+ induces the classical laddering degradation of DNA in vivo and that DNA cleavage is repaired after injection with Ca2+ under various Cd2+ concentrations. DNA cleavage caused by Cd2+ is due to the activation of deoxyribonuclease (DNase) and the accumulation of reactive oxygen species (ROS). Furthermore, Cd2+ destroys the antioxidant system, which diminishes the activities of superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD), causing an increase of the lipid peroxidation (LPO) level, respectively. However, after the liver is injected with Ca2+ under various Cd2+ concentrations, the DNase activity, the ROS generating rate and the LPO level are obviously reduced, the activities of SOD, CAT, and POD are greatly increased. At the same time, ROS production and removal recoves its balance. The results show that Ca2+ can relieve the toxicity of Cd2+ in silver crucian carp.

The improvement of spinach growth by nano-anatase TiO2 treatment is related to nitrogen photoreduction.

The improvement of spinach growth is proved to relate to N2 fixation by nano-anatase TiO2 in this study. The results show that all spinach leaves kept green by nano-anatase TiO2 treatment and all old leaves of control turned yellow white under culture with N-deficient solution. And the fresh weight, dry weight, and contents of total nitrogen, NH4(+), chlorophyll, and protein of spinach by nano-anatase TiO2 treatment presented obvious enhancement compared with control. Whereas the improvements of yield of spinach were not as good as nano-anatase TiO2 treatment under N-deficient condition, confirming that nano-anatase TiO2 on exposure to sunlight could chemisorb N2 directly or reduce N2 to NH3 in the spinach leaves, transforming into organic nitrogen and improving the growth of spinach. Bulk TiO2 effect, however, was not as significant as nano-anatase TiO2. A possible metabolism of the function of nano-anatase TiO2 reducing N2 to NH3 was discussed.

Effects of nano-anatase TiO2 on absorption, distribution of light, and photoreduction activities of chloroplast membrane of spinach.

The effects of nano-anatase TiO2 on light absorption, distribution, and conversion, and photoreduction activities of spinach chloroplast were studied by spectroscopy. Several effects of nano-anatase TiO2 were observed: (1) the absorption peak intensity of the chloroplast was obviously increased in red and blue region, the ratio of the Soret band and Q band was higher than that of the control; (2) the great enhancement of fluorescence quantum yield near 680 nm of the chloroplast was observed, the quantum yield under excitation wavelength of 480 nm was higher than the excitation wavelength of 440 nm; (3) the excitation peak intensity near 440 and 480 nm of the chloroplast significantly rose under emission wavelength of 680 nm, and F 480 / F 440 ratio was reduced; (4) when emission wavelength was at 720 nm, the excitation peaks near 650 and 680 nm were obviously raised, and F 650 / F 680 ratio rose; (5) the rate of whole chain electron transport, photochemical activities of PSII DCPIP photoreduction and oxygen evolution were greatly improved, but the photoreduction activities of PSI were a little changed. Together, the studies of the experiments showed that nano-anatase TiO2 could increase absorption of light on spinach chloroplast and promote excitation energy to be absorbed by LHCII and transferred to PSII and improve excitation energy from PSI to be transferred to PSII, thus, promote the conversion from light energy to electron energy and accelerate electron transport, water photolysis, and oxygen evolution.

Promotion of energy transfer and oxygen evolution in spinach photosystem II by nano-anatase TiO2.

Being a proven photocatalyst, nano-anatase is capable of undergoing electron transfer reactions under light. In previous studies we had proven that nano-anatase improved photosynthesis and greatly promoted spinach growth. The mechanisms by which nano-anatase promotes energy transfer and the conversion efficiency of the process are still not clearly understood. In the present paper, we report the results obtained with the photosystem II (PSII) isolated from spinach and treated by nano-anatase TiO2 and studied the effect of nano-anatase TiO2 on energy transfer in PSII by spectroscopy and on oxygen evolution. The results showed that nano-anatase TiO2 treatment at a suitable concentration could significantly change PSII microenvironment and increase absorbance for visible light, improve energy transfer among amino acids within PSII protein complex, and accelerate energy transport from tyrosine residue to chlorophyll a. The photochemical activity of PSII (fluorescence quantum yield) and its oxygen-evolving rate were enhanced by nano-anatase TiO2. This is viewed as evidence that nano-anatase TiO2 can promote energy transfer and oxygen evolution in PSII of spinach.

Effects of nano-anatase on spectral characteristics and distribution of LHCII on the thylakoid membranes of spinach.

In the article, we report that effects of nano-anatase on the spectral characteristics and content of light-harvesting complex II (LHCII) on the thylakoid membranes of spinach were investigated. The results showed that nano-anatase treatment could increase LHCII content on the thylakoid membranes of spinach and the trimer of LHCII; nano-anatase could enter the spinach chloroplasts and bind to PSII. Meanwhile, spectroscopy assays indicated that the absorption intensity of LHCII from nano-anatase-treated spinach was obviously increased in the red and the blue region, fluorescence quantum yield near 685 nm of LHCII was enhanced, the fluorescence excitation intensity near 440 and 480 nm of LHCII significantly rose and F 480/F 440 ratio was reduced. Oxygen evolution rate of PSII was greatly improved. Together, nano-anatase promoted energy transferring from chlorophyll (chl) b and carotenoid to chl a, and nano-anatase TiO2 was photosensitized by chl of LHCII, which led to enhance the efficiency of absorbing, transferring, and converting light energy.