Association of Monocyte-to-HDL Cholesterol Ratio with Endothelial Dysfunction in Patients with Type 2 Diabetes.

Aims: To explore the relationship between monocyte-to-HDL cholesterol ratio (MHR) and endothelial function in patients with type 2 diabetes (T2DM). Methods: 243 patients diagnosed with T2DM were enrolled in this cross-sectional study. Patients were divided into two groups by flow-mediated dilation (FMD) quintile as nonendothelial dysfunction (FMD ≥ 6.4%) and endothelial dysfunction (FMD < 6.4%). The relationship between MHR and FMD was analyzed using Spearman's correlation, partial correlation, and multiple logistic regression analysis. ROC curve was fitted to evaluate the ability of MHR to predict endothelial dysfunction. Results: Endothelial dysfunction was present in 193 (79%) patients. Patients with endothelial dysfunction had higher MHR (p < 0.05) than those without endothelial dysfunction. Furthermore, MHR had a significantly positive correlation with endothelial dysfunction (r = 0.17, p < 0.05), and the positive association persisted even after controlling for confounding factors (r = 0.14, p < 0.05). Logistic regression showed that MHR was an independent contributor for endothelial dysfunction (OR: 1.35 (1.08, 1.70), p < 0.05) and the risk of endothelial dysfunction increases by 61% with each standard deviation increase in MHR (OR: 1.61 (1.12, 2.30), p < 0.05) (model 1). After adjusting for sex, age, BMI, disease course, hypertension, smoking, and drinking (model 2) as well as HbA1c, HOMA-IR, C-reactive protein, and TG (model 3), similar results were obtained. In ROC analysis, the area of under the ROC curve (AUC) for MHR was 0.60 (95% CI 0.52-0.69, p < 0.05). Conclusion: MHR was independently associated with endothelial dysfunction in T2DM patients. It could be a new biomarker for vascular endothelial function assessment.

In vitro promotion of SDF-1α on the migration and proliferation of C-kit+ cardiac stem cells in neonatal mice.

The aim of this study was to explore the In Vitro effects of stromal-derived factor-1α (SDF-1α) on the migration and proliferation of c-kit+ cardiac stem cells. The lentivirus containing SDF-1α (LV-SDF-1α) was constructed. Primary myocardial fibroblasts were transfected by LV-SDF-1α, followed by primary culture of cardiac tissue cells and separation of c-kit+ cardiac stem cells with a flow cytometer, in order to investigate the effects of SDF-1α on the migration and proliferation of c-kit+ cardiac stem cells using cell co-culture, immunofluorescence and EdU tracing technologies. The results showed that myocardial fibroblasts could secrete SDF-1α after the transfection with LV-SDF-1α. High-purity c-kit+ cardiac stem cells were obtained through flow cytometry sorting and the positive rate was about 40%. The c-kit+ cardiac stem cells cultured In Vitro could be differentiated into cTnT positive cardiomyocyte-like cells. After co-culture of myocardial fibroblasts and c-kit+ cardiac stem cells transfected with lentivirus, SDF-1α might increase the migration of c-kit+ cardiac stem cells, but SDF-1α did not promote the proliferation of c-kit+ cardiac stem cells. In conclusion, the myocardial fibroblasts transfected with lentivirus can highly express SDF-1α, c-kit+ cardiac stem cells can be differentiated into cTnT positive cardiomyocyte-like cells and SDF-1α can effectively enhance the migration of c-kit+ cardiac stem cells but fails to stimulate the proliferation.

Fibroblast growth factor 2 acts as an upstream regulator of inhibition of pulmonary fibroblast activation.

Fibroblast growth factor (FGF) signaling plays a crucial role in lung development and repair. Fibroblast growth factor 2 (FGF2) can inhibit fibrotic gene expression and suppress the differentiation of pulmonary fibroblasts (PFs) into myofibroblasts in vitro, suggesting that FGF2 is a potential target for inhibiting pulmonary fibrosis. To gain deeper insights into the molecular mechanism underlying FGF2-mediated regulation of PFs, we performed mRNA sequencing analysis to systematically and globally uncover the regulated genes and biological functions of FGF2 in PFs. Gene Ontology analysis revealed that the differentially expressed genes regulated by FGF2 were enriched in multiple cellular functions including extracellular matrix (ECM) organization, cytoskeleton formation, ß-catenin-independent Wnt signaling pathway, supramolecular fiber organization, epithelial cell proliferation, and cell adhesion. Gene Set Enrichment Analysis and cellular experiments confirmed that FGF2 can suppress ECM and actin filament organization and increase PFs proliferation. Taken together, these findings indicate that FGF2 acts as an upstream regulator of the inhibition of PFs activation and may play a regulatory role in pulmonary fibrosis.

Effects of Steel Slag Powder Content and Curing Condition on the Performance of Alkali-Activated Materials Based UHPC Matrix.

The accumulation of steel slag and other industrial solid wastes has caused serious environmental pollution and resource waste, and the resource utilization of steel slag is imminent. In this paper, alkali-activated ultra-high-performance concrete (AAM-UHPC) was prepared by replacing ground granulated blast furnace slag (GGBFS) powder with different proportions of steel slag powder, and its workability, mechanical properties, curing condition, microstructure, and pore structure were investigated. The results illustrate that the incorporation of steel slag powder can significantly delay the setting time and improve the flowability of AAM-UHPC, making it possible for engineering applications. The mechanical properties of AAM-UHPC showed a tendency to increase and then decrease with the increase in steel slag dosing and reached their best performance at a 30% dosage of steel slag. The maximum compressive strength and flexural strength are 157.1 MPa and 16.32 Mpa, respectively. High-temperature steam or hot water curing at an early age was beneficial to the strength development of AAM-UHPC, but continuous high-temperature, hot, and humid curing would lead to strength inversion. When the dosage of steel slag is 30%, the average pore diameter of the matrix is only 8.43 nm, and the appropriate steel slag dosage can reduce the heat of hydration and refine the pore size distribution, making the matrix denser.

Mechanical and Microstructural Characteristics of Calcium Sulfoaluminate Cement Exposed to Early-Age Carbonation Curing.

The early-age carbonation curing technique is an effective way to improve the performance of cement-based materials and reduce their carbon footprint. This work investigates the early mechanical properties and microstructure of calcium sulfoaluminate (CSA) cement specimens under early-age carbonation curing, considering five factors: briquetting pressure, water-binder (w/b) ratio, starting point of carbonation curing, carbonation curing time, and carbonation curing pressure. The carbonization process and performance enhancement mechanism of CSA cement are analyzed by mercury intrusion porosimetry (MIP), thermogravimetry and derivative thermogravimetry (TG-DTG) analysis, X-ray diffraction (XRD), and scanning electron microscope (SEM). The results show that early-age carbonation curing can accelerate the hardening speed of CSA cement paste, reduce the cumulative porosity of the cement paste, refine the pore diameter distribution, and make the pore diameter distribution more uniform, thus greatly improving the early compressive strength of the paste. The most favorable w/b ratio for the carbonization reaction of CSA cement paste is between 0.15 and 0.2; the most suitable carbonation curing starting time point is 4 h after initial hydration; the carbonation curing pressure should be between 3 and 4 bar; and the most appropriate time for carbonation curing is between 6 and 12 h.

Influence of Different Lithium Compounds on Hydration and Mechanical Properties of Calcium Sulfoaluminate Cement.

This work investigated the influence of three different lithium compounds, lithium carbonate (Li2CO3), lithium sulfate (Li2SO4) and lithium chloride (LiCl), on the hydration and mechanical properties of calcium sulfoaluminate (CSA) cement mixtures. Five concentrations of Li+, 0, 0.05, 0.11, 0.16 and 0.22 mmol/g of cement, were chosen, and then the proportions (by mass) of three lithium compounds were determined. Compressive strengths at 8 h, 24 h and 28 days were tested. Meanwhile, an early hydration heat test, thermogravimetric (TG) analysis, X-ray diffraction (XRD) and scanning electron microscope (SEM) techniques were performed to study the influences of different lithium compounds on properties of CSA cement mixtures. The experimental results show that three lithium compounds can all accelerate the early hydration process of CSA cement. There is not a remarkable difference on the properties of CSA cement pastes with a different content of Li+. The anion of lithium compounds can also affect the properties of CSA cement pastes, the accelerating effects of LiCl and Li2SO4 are more significant than that of Li2CO3, but there is not a distinct difference between LiCl and Li2SO4.

Protective effect of flavonoids from Rosa roxburghii Tratt on myocardial cells via autophagy.

The aim of this study is to explore the effect of flavonoids from Rosa roxburghii Tratt (FRRT) on doxorubicin (DOX)-induced autophagy of myocardial cells. Primary isolation and culture of myocardial cells and H9C2 myocardial cell lines from 1 to 3-day-old rats were performed, myocardial cells were incubated using 5 µmol/L DOX and a cardiotoxicity model was established, intervention was conducted via FRRT, and the ultrastructure of myocardial cells was observed under a transmission electron microscope. The expressions of LC3-II and P62 proteins were detected through immunofluorescence and Western blotting. The ultrastructure showed a large quantity of autophagic vacuoles of the cells in DOX group with poor cell state. After the FRRT intervention, only a small quantity of autophagic vacuoles appeared in the myocardial cells, and there were many coarse microvilli on the cell surface. The expression of P62 protein was reduced in DOX group, while that in FRRT group was increased (p < 0.01). In conclusion, FRRT exerts a protective effect in the DOX-induced cardiotoxicity by down-regulating DOX-induced autophagy of myocardial cells.

Continuous monitoring for leaching of calcium sulfoaluminate cement pastes incorporated with ZnCl2 under the attacks of chloride and sulfate.

Ionic zinc is considered as an environmental pollutant. This work systematically investigated leaching mechanisms of calcium sulfoaluminate cement (CSA) pastes incorporated with/without ZnCl2 under the attacks of chloride and/or sulfate. The leaching behaviors of CSA pastes in the leaching solution are in-situ and continuously monitored by innovative non-contact electrical impedance measurement (NCEIM) and pH meter. The dissolution and diffusion during the leaching process are experimentally identified. Other techniques are also performed to verify the finding of NCEIM: the ion chromatograph and inductively coupled plasma optical emission spectrometer reveal the leaching or decomposition sequence of CSA pastes during the leaching process. Besides, results from XRD and SEM techniques demonstrate that main solid products in CSA pastes are ettringite and calcium monosulfoaluminate hydrates. The incorporation of Zn in the pastes has great impact on the decomposition of CSA pastes in the temperature elevation. External chloride and/or sulfate attacks significantly alter the pore structure of CSA pastes during the leaching process.

SDF-1α promotes repair of myocardial ischemic necrosis zones in rats.

OBJECTIVE: To explore the repair effect of stromal cell-derived factor-1α (SDF-1α) on myocardial ischemic necrosis zones. METHODS: Lentivirus (LV-SDF-1α-GFP) containing SDF-1α target gene was established, the separated and cultured neonatal rat cardiac fibroblasts were transfected, and caudal intravenous injection of isoproterenol was conducted to prepare a rat model of myocardial ischemia. Small animal ultrasound was used to evaluate the effect on cardiac functions. Morphology and immunofluorescence were used to observe the change of ischemic necrosis zones and expressions of stem cellular markers c-kit, CD34, nkx2.5, and nanog, and a quantitative analysis was performed. RESULTS: The established LV-SDF-1α-GFP was used to transfect myocardial fibroblasts which presented GFP green fluorescent expression and could secrete SDF-1α. The small animal ultrasound system showed that rat cardiac functions of the lentivirus group and cell group were improved to different degrees, myocardial ischemic necrosis zones of lentivirus group and cell group were reduced, and differences had statistical significances (P<0.05). Immunofluorescence showed that expressions of stem cellular markers c-kit, CD34, nkx2.5 and nanog in myocardial tissue ischemic zones in both the lentivirus group and cell group increased, and differences through inter-group comparison had statistical significances (P<0.05). CONCLUSION: SDF-1α can promote migration and proliferation of stem cells into the myocardial ischemic necrosis zone, participate in repair of the myocardial necrosis zone, and improve cardiac function.

A new and important relationship between miRNA-147a and PDPK1 in radiotherapy.

It was found that the expression level of miR-147a was significantly increased and the pathway of PI3K/AKT was dramatically inhibited after radiation. In view of the relationship between miRNA and target genes, we put forward the question, what is the relationship between PI3K/AKT and miR-147a? In order to find the answer to the question, we used bioinformatics techniques to analyze the relationship between miR-147 (a or b) and PI3K/AKT signaling pathway. miR-147a overexpression plasmid and PDPK1 3'UTR luciferase reporter gene plasmid were constructed. Dual luciferase reporter gene system validation experiments were carried out on miR-147a and PDPK1 relationship. The verification experiments were also carried out. Bioinformatics analysis showed that there is a miR-147a binding site in the non-coding region (3'UTR) of PDPK1. In the experimental groups transfected with wild type PDPK1 gene of 3'UTR plasmid, the luciferase activity decreased (or increased) significantly in miR-147a (or inhibitor) group compared with miR-NC (or anti-miR-NC); There was no significant difference between the miR-147a group (or inhibitor) and the miR-NC group (or anti-miR-NC) in the transfection of PDPK1-3'UTR-Mut gene vector. PDPK1 was a target gene for direct regulation of miR-147a downstream. Verifying test results showed that the expression of PDPK1 mRNA and protein was reduced after overexpression of miR-147a, which was up-regulated after silencing miR-147a in TC, and V79 cells. These results suggest that miR-147a could be involved in the regulation of PDPK1 transcription by binding to the target site in PDPK1 mRNA 3'UTR, and then regulated AKT.

Flavonoids of Rosa roxburghii Tratt Exhibit Anti-Apoptosis Properties by Regulating PARP-1/AIF.

Radioprotection is an important approach to reduce the side-effects of radiotherapy. The radioprotective effect of the flavonoids of Rosa roxburghii Tratt (FRT) has been confirmed, and the mechanism has been identified as theBcl-2/caspase-3/PARP-1 signaling pathway. In this study, we investigated the effects of FRT on the intercellular adhesion molecule (ICAM), and vascular cell adhesion protein (VCAM) in addition to apoptosis-related proteins such as Bax/Bcl-2, p-ERK/ERK, p-p53/p53, and p-p38/p38. In the present study, we focused on the effect of FRT on PARP-1/AIF. Ionizing radiation triggered the activation of PARP-1 and AIF translocation from the mitochondrion to the nucleus. The inhibition of PARP-1/AIF signaling pathway by FRT was investigated. Our results showed that the expressions of Bax/Bcl-2, p-ERK/ ERK, p-p53/p53, and p-p38/p38 were decreased after FRT treatment compared with the radiation-treated group. FRT inhibited PARP-1 activation to inhibit AIF translocation from mitochondrion to nucleus. Pretreatment with FRT diminished the comet's tail and reduced fragments in six Gy-irradiated thymocytes compared with the irradiated cells without FRT treatment. We conclude that FRT enhanced radioprotection at least partially by regulating PARP-1/AIF to reduce apoptosis. J. Cell. Biochem. 118: 3943-3952, 2017. © 2017 Wiley Periodicals, Inc.

Activating AKT to inhibit JNK by troxerutin antagonizes radiation-induced PTEN activation.

Radiotherapy is one of the most effective non-surgical treatments for many tumors. However, radiation damage remains a major negative consequence of radiotherapy. At present, radio-protective effect of troxerutin has been confirmed, but the mechanism of this radioprotection has not been elucidated. Here, this study showed that troxerutin protected thymus tissue of irradiated mice, and its radio-protective effect on thymocytes was significant in the range of 0.625-10µg/ml. Troxerutin significantly inhibited apoptosis of irradiated thymocytes at the concentration of 10µg/ml. Computer-aided drug design was used to investigate potential candidate targets for troxerutin, and an excellent correlation was identified between troxerutin and AKT (Pharm mapper and KEGG signal pathway). Troxerutin inhibited the activation of PTEN to stimulate AKT, which in turn prevented the activation of JNK to protect cells. Our results showed that troxerutin enhanced radioprotection at least partially by activating AKT to inhibit the activation of JNK.

Flavonoids of Rosa roxburghii Tratt exhibit radioprotection and anti-apoptosis properties via the Bcl-2(Ca(2+))/Caspase-3/PARP-1 pathway.

The objective of our study was to assess the radioprotective effect of flavonoids extracted from Rosa roxburghii Tratt (FRT) and investigate the role of Bcl-2(Ca(2+))/Caspase-3/PARP-1 pathway in radiation-induced apoptosis. Cells and mice were exposed to (60)Co γ-rays at a dose of 6 Gy. The radiation treatment induced significant effects on tissue pathological changes, apoptosis, Ca(2+), ROS, DNA damage, and expression levels of Bcl-2, Caspase-3 (C-Caspase-3), and PARP-1. The results showed that FRT acted as an antioxidant, reduced DNA damage, corrected the pathological changes of the tissue induced by radiation, promoted the formation of spleen nodules, resisted sperm aberration, and protected the thymus. FRT significantly reduced cell apoptosis compared with the irradiation group. The expression of Ca(2+) and C-Caspase-3 was decreased after FRT treatment compared with the radiation-treated group. At the same time, expression of prototype PARP-1 and Bcl-2 increased, leading to a decrease in the percentage of apoptosis cells in FRT treatment groups. We conclude that FRT acts as a radioprotector. Apoptosis signals were activated via the Bcl-2(Ca(2+))/Caspase-3/PARP-1 pathway in irradiated cells and FRT inhibited this pathway of apoptosis by down-regulation of C-Caspase-3 and Ca(2+) and up-regulation of prototype PARP-1 and Bcl-2.

Surface modification of PLGA nanoparticles with biotinylated chitosan for the sustained in vitro release and the enhanced cytotoxicity of epirubicin.

In this study, poly(d,l-lactide-co-glycolide) nanoparticles (PLGA NPs) with biotinylated chitosan (Bio-CS)-surface modification were prepared to be usded as a tumor-targeted and prolonged delivery system for anticancer drugs. Epirubicin (EPB), as a model drug, was encapsulated into Bio-CS surface modified PLGA (Bio-CS-PLGA) NPs with a drug encapsulation efficiency of 84.1 ± 3.4%. EPB-loaded Bio-CS-PLGA NPs were spherical shaped, and had a larger size and higher positive zeta potential compared to the unmodfied EPB-loaded PLGA NPs. The in vitro drug releases showed that EPB-loaded Bio-CS-PLGA NPs exhibited relatively constant drug release kinetics during the first 48 h and the drug burst release significantly decreased in comparison to the unmodified PLGA NPs. The results of MTS assays showed that Bio-CS-PLGA NPs markedly increased the cytotoxicity of EPB, compared to both the unmodified PLGA NPs and the CS-PLGA NPs. The uptakes of NPs in human breast cancer MCF-7 cells were evaluated by the flow cytometry and the confocal microscope. The results revealed that Bio-CS-PLGA NPs exhibited a greater extent of cellular uptake than the unmodified PLGA NPs and CS-PLGA NPs. Moreover, the cellular uptake of Bio-CS-PLGA NPs was evidently inhibited by the endocytic inhibitors and the receptor ligand, indicating that biotin receptor-mediated endocytosis was perhaps involved in the cell entry of Bio-CS-PLGA NPs. In MCF-7 tumor-bearing nude mice, EPB-loaded Bio-CS-PLGA NPs were efficiently accumulated in the tumors. In summary, Bio-CS-PLGA NPs displayed great potential for application as the carriers of anticancer drugs.

Microtubule-targetable fluorescent probe: site-specific detection and super-resolution imaging of ultratrace tubulin in microtubules of living cancer cells.

Tubulins in microtubules have been recognized as potential targets in cancer chemotherapy for several years. However, their detection and imaging in living cells, especially following exposure to anticancer drugs, remains difficult to achieve. This difficulty is due to the very small cross section of microtubules and the very small changes in tubulin concentration involved. Photoswitchable fluorescent probes combined with the "super-resolution" fluorescence imaging technique present an exciting opportunity for site-specific detection and super-resolution imaging of specific microscopic populations, such as tubulin. In this study, a tubulin specific photoswitchable fluorescent probe (Tu-SP), that labels and detects ultratrace levels of tubulin in microtubules of living biosystems, was designed and evaluated. To realize super-resolution fluorescence imaging, the spiropyran derivative (SP), a classic photoswitch, was introduced to Tu-SP as a fluorophore. To detect ultratrace tubulin, Tu-SP employed the tubulin inhibitor, alkaloid colchicine (Tu), as a recognition unit. Tu-SP exhibited nearly nonintrinsic fluorescence before binding to tubulin, even if there were divalent metal ions and 375 nm lasers, respectively. After binding to tubulin, a dramatic increase in fluorescence was detected within milliseconds when irradiated at 375 nm, this increase is a result of the transformation of Tu-SP into a colored merocyanine (Tu-SP-1) with fluorescence. Tu-SP was successfully used for site-specific imaging of tubulin at a resolution of 20 ± 5 nm in microtubules of living cancer cells. More importantly, the probe was suitable for site-specific and quantitative detection of trace tubulin in microtubules of living biological samples.

Flavonoids of Rosa roxburghii Tratt act as radioprotectors.

BACKGROUND: To study the radioprotective effects of flavonoids from Rosa roxburghii Tratt (FRT). MATERIALS AND METHODS: The radioprotective effects of FRT were investigated by examining cell viability, 30-day survival of mice and the number of colony-forming units in spleen (CFU-S) after total-body 60Co irradiation. RESULTS: The survival rates of irradiated cells gradually increased with increasing concentrations of FRT. The survival rate was the highest at 87% with a concentration of 30 µg/mL. Pretreatment with FRT was needed to realize its radioprotective activity in mice at the dose of 60 mg/kg. With the increasing doses of 30 mg/kg, 60 mg/kg and 120 mg/kg, the numbers of CFU-S increased, and were significantly different compared with the control group. CONCLUSIONS: Pretreatment with FRT prior to irradiation resulted in significantly higher cell survival at 24 h after 5 Gy radiation, increased 30-day survival in mice after exposure to a potentially lethal dose of 8 Gy, and resulted in a higher number of CFU-S in mice after exposure to a dose of 6 Gy. These results collectively indicate that FRT is an effective radioprotective agent.

[X-ray hardening correction for ICT in testing workpiece].

Since energy spectrum of X-ray is polychromatic source in X-ray industrial computerized tomography, the variation of attenuation coefficient with energy leads to the lower energy of X-ray radiation being absorbed preferentially when X-ray is transmitting the materials. And the higher the energy of X-ray, the lower the attenuation coefficient of X-ray. With the increase in the X-ray transmission thickness, it becomes easier for the X-ray to transmit the matter. Thus, the phenomenon of energy spectrum hardening of X-ray takes place, resulting from the interaction between X-ray and the materials. This results in false images in the reconstruction of X-ray industrial computerized tomography. Therefore, hardening correction of energy spectrum of X-ray has to be done. In the present paper, not only is the hardening phenomenon of X-ray transmitting the materials analyzed, but also the relation between the X-ray beam sum and the transmission thickness of X-ray is discussed. And according to the Beer law and the characteristics of interaction when X-ray is transmitting material, and by getting the data of X-ray beam sum, the relation equation is fitted between the X-ray beam sum and X-ray transmission thickness. Then, the relation and the method of equivalence are carried out for X-ray beam sum being corrected. Finally, the equivalent and monochromatic attenuation coefficient fitted value for X-ray transmitting the material is reasoned out. The attenuation coefficient fitted value is used for product back-projection image reconstruction in X-ray industrial computerized tomography. Thus, the effect caused by X-ray beam hardening is wiped off effectively in X-ray industrial computerized tomography.

[Beam hardening simulated correction research for X-ray TICT in testing composites workpiece].

In X-ray TICT, when X-ray is transmitted in the materal, the phenomenon of energy spectrum hardening takes place, resulting in artifacts. Thus, hardening correction has to be done. In the present paper, the phenomenon of X-ray beam hardening resulting in analyized, and the relation between the X-ray beam sum and the transmission thickness in testing composites workpiece is discussed. According to the Beer law and the characteristics of the interaction between X-ray and the material, and getting the data of X-ray beam sum, the relation equation between the beam sum and transmission thickness is simulated firstly, and testing composites workpiece. Then, the relation and the method of equivalence are carried out between the equivalent transmission thickness and the transmission thickness for X-ray beam sum being corrected for monochromatic ray beam. Finally, the attenuation coefficient beam hardening simulated value for X-ray equivalent monochromatic is reasoned out in testing composites workpiece. Then, the attenuation coefficient simulated value that has been corrected is used for product back-projection reconstruction. Thus, the effect caused by X-ray beam hardening is wipped off effectively in testing composites workpiece.

[Hardening correction model of energy spectrum for X-ray TICT in testing composites workpiece].

In the case of a polychromatic source in X-ray TICT, the variation of attenuation coefficient with energy leads to low energy radiation being absorbed preferentially. In other words, the higher the energy, the lower the attenuation coefficient. With the transmission thickness augmenting, it is easier for X-ray to transmit the matter. The phenomenon is energy spectrum hardening. Thus, hardening correction has to be done. In the present paper, not only is energy spectrum hardening analyzed by theory and the relation stated between attenuation coefficient and transmission thickness in testing composites workpiece, but also the precise accurate theory model for hardening correction of energy spectrum and theory method are reasoned out in testing composites workpiece, which results from Beer's law and the characteristics of X-ray interaction with composites. Then, the attenuation coefficient that has been corrected is used for product back-projection reconstruction. Thus, the effect caused by X-ray beam hardening is wipped out effectively in testing composites workpiece.