Neurological Dysfunction and Serum Levels of IL-6 and IL-1ß in Patients Undergoing Isoflurane Inhalation Anesthesia: A Correlation Study.

Objective: This study aims to explore the association between neurological dysfunction and serum levels of Interleukin-6 (IL-6) and Interleukin-1ß (IL-1ß) in patients undergoing isoflurane inhalation anesthesia. Methods: This prospective observational study enrolled a total of 88 patients who underwent isoflurane anesthesia, between April 2019 and April 2020 in our hospital's operating room. The Mini-Mental State Examination scale (MMSE) was administered on the first preoperative day (T0), the 1st postoperative day (T1), the 3rd postoperative day (T2), and the 7th postoperative day (T3). Based on the MMSE score obtained on the 1st postoperative day, patients were categorized into the neurological dysfunction group (n = 23) and the normal group (n = 65). Serum levels of IL-6 and IL-1ß were measured at T0, T1, T2, and T3, and their relationship with MMSE scores was analyzed. Results: Compared to the normal group, the neurological dysfunction group exhibited significantly higher levels of serum IL-6 and IL-1ß at all time points except T0, accompanied by notably lower MMSE scores (P < .001). Combined diagnostic parameters, including area under the curve (AUC) value, sensitivity, and specificity, showed improved performance compared to individual tests. Pearson correlation analysis revealed a negative correlation between serum IL-6 and IL-1ß levels and MMSE scores (r = -0.719, -0.408, all P < .05). Conclusions: Our findings highlight a correlation between neurological dysfunction and serum IL-6 and IL-1ß levels in patients undergoing isoflurane inhalation anesthesia. These cytokines could serve as valuable indicators for the early detection of neurological dysfunction following anesthesia.

[Unsaturated fatty acid of Actinidia chinesis planch seed oil protects against pulmonary fibrosis by inhibiting collagen synthesis via down-regulating connective tissue growth factor (CTGF) expression in rats].

Objective To observe the role of connective tissue growth factor (CTGF) and collagen synthesis in anti-pulmonary fibrosis (PF) by Kiwi fruit essence(unsaturated fatty acid of actinidia chinesis planch seed oil)in rats. Methods Sixty male SD rats were randomly divided into control group, model group, Kiwi fruit essence (60, 120, 240 mg/kg) treatment groups, and 5 mg/kg prednisone acetate group, with 10 animals in each group. Rats in control group were intratracheally administered with 9 g/L sodium chloride solution, and animals in other groups were intratracheally administered with bleomycin A5 to establish PF model. From the second day on, rats in the latter 4 groups were intragastrically treated with Kiwi fruit essence of 60, 120 and 240 mg/kg and prednisone acetate of 5 mg/kg, respectively. Rats in control and model groups were treated with 9 g/L sodium chloride solution once a day. All rats were sacrificed on day 28, and then pulmonary tissues were removed. The extent of PF lesions were evaluated using HE and Masson staining. The contents of hydroxyproline (HYP) were measured by a commercial kit. The mRNA expressions of CTGF and α-smooth muscle actin (α-SMA) in pulmonary tissues was detected by quantitative real-time PCR. The protein expressions of CTGF, α-SMA, collagen type 1 (Col1) and Col3 were measured by Western blotting. The protein levels of CTGF were analyzed using immunohistochemical staining. Results Compared with the model group, the alveolitis and PF extent in 60, 120, 240 mg/kg Kiwi fruit essence treatment groups as well as 5 mg/kg prednisone acetate group were significantly alleviated, and the content of HYP and the expression of CTGF, α-SMA, Col1 and Col3 decreased. The changes of above indicators were dose-dependent among the (60, 120, 240) mg/kg Kiwi fruit essence treatment groups. Moreover, the above indicators were found higher in (60, 120) mg/kg Kiwi fruit essence treatment groups than those in 5 mg/kg prednisone acetate group, which, however, showed no significantly difference between 240 mg/kg Kiwi fruit essence treatment group and 5 mg/kg prednisone acetate group. Conclusion Kiwi fruit essence down-regulates CTGF expression and decreases the levels of α-SMA, leading to inhibition of Col1 and Col3 synthesis and alleviation of PF.

The Role of Oxymatrine in Amelioration of Acute Lung Injury Subjected to Myocardial I/R by Inhibiting Endoplasmic Reticulum Stress in Diabetic Rats.

BACKGROUND: Oxymatrine (OMT) is the primary pharmacological component of Sophora flavescens Aiton., which has been shown to possess potent antifibrotic, antioxidant, and anti-inflammatory activities. The aim of the present study was to clarify the protective mechanism of OMT on acute lung injury (ALI) subjected to myocardial ischemia/reperfusion (I/R). METHODS: A myocardial I/R-induced ALI model was achieved in diabetic rats by occluding the left anterior descending coronary artery for 1 h, followed by reperfusion for 1 h. The levels of inflammatory factors (tumor necrosis factor-α, interleukin- (IL-) 6, and IL-17) in bronchoalveolar lavage fluid were assessed using commercially available kits. The index of myocardial injury, including the detection of cardiac troponin I (cTnI), cardiac troponin T (cTnT), lactate dehydrogenase (LDH), and creatine kinase-MB (CK-MB), was also determined using commercially available kits. Hematoxylin and eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were used to identify histological changes. The expression levels of endoplasmic reticulum chaperone BiP (GRP78), DNA damage-inducible transcript 3 protein (CHOP), eukaryotic translation initiation factor 2-alpha kinase 3 (PERK), inositol dependent enzyme 1α (IRE1α), ATF6, caspase-3, -9, and-12, Bcl-2, and Bax were determined by Western blotting. The mRNA expression levels of GRP78 and CHOP were detected by reverse transcription-quantitative PCR. RESULTS: Myocardial I/R increased the levels of cTnI, cTnT, LDH, and CK-MB in diabetic rats. Damaged and irregularly arranged myocardial cells were also observed, as well as more serious ALI with higher lung injury scores and WET/DRY ratios and lower PaO2. Moreover, the expression of key proteins of endoplasmic reticulum stress (ERS) was increased by I/R injury, including phosphorylated- (p-) PERK, p-IRE1ɑ, and ATF6, as well as decreased levels of apoptosis. These effects were all significantly reversed by OMT treatment. CONCLUSIONS: OMT protects against ALI subjected to myocardial I/R by inhibiting ERS in diabetic rats.

[Unsaturated fatty acid of Actinidia chinesis planch seed oil (kiwi fruit essence) inhibits growth and metastasis of transplanted tumor in lung adenocarcinoma mice by up-regulating EHD2 expression].

Objective To observe the role of Eps15 homology domain containing protein 2 (EHD2) in the inhibitive effects of unsaturated fatty acid of Actinidia chinesis planch seed oil (kiwi fruit essence) on the growth and metastasis of transplanted tumor in lung adenocarcinoma mice. Methods 32 C57BL/6J mice bearing Lewis lung adenocarcinoma cells were randomly divided into the control group, 60, 120 and 240 mg/kg kiwi fruit essence treatment groups. Each group included 8 animals. From the fourth day after innoculation, the mice in the control group were intragastrically treated with normal saline, and the mice were intragastrically treated with 60, 120 or 240 mg/kg kiwi fruit essence in the corresponding kiwi fruit essence treatment groups. After measuring the volume of transplanted tumors, all mice were sacrificed on day 24, and their pulmonary tissues were then removed to observe tumor metastasis. The transplanted tumors were exfoliated and weighed to calculate the metastasis inhibition rate and tumor inhibition rate. The protein expression level of EHD2 in the transplanted tumors was detected by immunohistochemistry and Western blotting. The mRNA expression level of EHD2 in the transplanted tumors was measured using real-time quantitative PCR. Results Compared with the control group, the growth, volume, quality and number of lung metastasis nodules of the subcutaneous transplanted tumors significantly decreased, and tumor inhibition rates and metastasis inhibition rates increased in 60, 120, 240 mg/kg kiwi fruit essence treatment groups. The protein and mRNA level of EHD2 in the subcutaneous transplanted tumors went up. Compared with the 60 mg/kg kiwi fruit essence treatment group, the above indicators were significantly improved in 120 and 240 mg/kg kiwi fruit essence treatment groups in a dose-dependent manner. Conclusion Kiwi fruit essence can up-regulate EHD2 expression, thereby inhibiting the growth and metastasis of lung adenocarcinoma transplantation tumor in mice.

Selenium Yeast Alleviates Ochratoxin A-Induced Apoptosis and Oxidative Stress via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in the Kidneys of Chickens.

The purpose of this study was to investigate the protective effect and mechanism of yeast selenium (Se-Y) on ochratoxin- (OTA-) induced nephrotoxicity of chickens. A total of 80 one-day-old healthy chickens were randomly divided into 4 equal groups: control, OTA (50 µg/kg OTA), Se-Y (0.4 mg/kg Se-Y), and OTA+Se-Y (50 µg/kg OTA+0.4 mg/kg Se-Y). In the OTA chickens, differences in body weight, kidney coefficient, biochemical histological analysis, antioxidant capability, and the expression levels of the PI3K/AKT and Nrf2/Keap1 signaling pathway-related genes were observed. The levels of total superoxide dismutase (T-SOD), antioxidant capacity (T-AOC), catalase (CAT), and glutathione (T-GSH) significantly decreased, but the malondialdehyde (MDA) level of the kidneys significantly increased in the OTA treatment group. More importantly, treatment with Se-Y improved the antioxidant enzyme activities within the kidneys of chickens exposed to OTA. In addition, administration of OTA resulted in apoptosis and was associated with decreased expression of AKT, PI3K, and Bcl-2, which in turn enhanced expression of Caspase3, Bax, and P53. However, Se-Y improved the antioxidant defense system through activation of the Nrf2/Keap1 signaling pathway. Gene expression of Nrf2 and its target genes (HO-1, GSH-px, GLRX2, MnSOD, and CAT) was downregulated following OTA exposure. Conversely, Se-Y treatment resulted in a significant upregulation of the same genes. Besides, significant downregulations of protein expression of HO-1, CAT, MnSOD, Nrf2, and Bcl-2 and a significant upregulation of Caspase3 and Bax levels were observed after contaminated with OTA. Notably, OTA-induced apoptosis and oxidative damage in the kidney of chickens were reverted back to normal level in the OTA+Se-Y group. Taken together, the data suggest that Se-Y alleviates OTA-induced nephrotoxicity in chickens, possibly through the activation of the PI3K/AKT and Nrf2/Keap1 signaling pathways.

Preventive effect of hesperidin modulates inflammatory responses and antioxidant status following acute myocardial infarction through the expression of PPAR­Î³ and Bcl­2 in model mice.

Hesperetin is the main pharmacological ingredient of fruit of the citrus family, rutaceae. It is a flavanone, which has potent antioxidation and anti­inflammatory activities. The present study investigated the preventive effect of hesperidin in the modulation of acute myocardial infarction (AMI)­induced inflammatory responses and antioxidant status in a mouse model. The levels of creatine kinase­MB, tumor necrosis factor (TNF­α), interleukin (IL)­1ß, IL­6, monocyte chemoattractant protein 1 (MCP­1), intercellular adhesion molecule 1 (ICAM­1), malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and caspase­3/9 were measured using ELISA kits. Western blot analysis analyzed p53 and B­cell lymphoma 2 (Bcl­2)­associated X protein/Bcl­2, and induced the expression of peroxisome proliferator­activated receptor­Î³ (PPAR­Î³). Hesperidin markedly decreased the myocardial infarction area, heart weight/body weight ratio and activity of creatine kinase­MB in AMI mice. Hesperidin treatment caused a significant decrease in the levels of TNF­α, IL­1ß, IL­6, MCP­1, ICAM­1, MDA, CAT, SOD and caspase­3/9 in mice with AMI. Hesperidin also significantly suppressed the protein expression levels of p53 and Bax/Bcl­2, and induced the expression of peroxisome proliferator­activated receptor­Î³ (PPAR­Î³) in mice with AMI. The preventive effect of hesperidin modulated the inflammatory response and antioxidant status following AMI through downregulation of the expression of PPAR­Î³ and Bcl­2 in the model mice.

The Protective Effect of Selenium on Chronic Zearalenone-Induced Reproductive System Damage in Male Mice.

This study aims to explore the protective effect of selenium (Se) on chronic zearalenone (ZEN)-induced reproductive system damage in male mice and the possible protective molecular mechanism against this. The chronic ZEN-induced injury mouse model was established with the continuous intragastric administration of 40 mg/kg body mass (B.M.) ZEN for 28 days. Then, interventions with different doses (0.1, 0.2, and 0.4 mg/kg B.M.) of Se were conducted on mice to analyse the changes in organ indexes of epididymis and testis, antioxidant capability of testis, serum level of testosterone, sperm concentration and motility parameters, and the expression levels of apoptosis-associated genes and blood testis barrier- (BTB) related genes. Our results showed that Se could greatly improve the ZEN-induced decrease of epididymis indexes and testis indexes. Results also showed that the decrease in sperm concentration, sperm normality rate, and sperm motility parameters, including percentage of motile sperm (motile), tropism percentage (progressive) and sperm average path velocity (VAP), caused by ZEN were elevated upon administration of the higher dose (0.4 mg/kg) and intermediate dose (0.2 mg/kg) of Se. Selenium also significantly reduced the content of malondialdehyde (MDA) but enhanced the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the testis tissue. Further research demonstrated that ZEN increased the level of mRNA expression of BCL2-associated X protein (Bax) and caspase 3 (Casp3), decreased the level of mRNA expression of B cell leukemia/lymphoma 2 (Bcl2), vimentin (Vim) and cadherin 2 (Cdh2), whereas the co-administration of Se reversed these gene expression levels. Our results indicated that high levels of Se could protect against reproductive system damage in male mice caused by ZEN and the mechanism might such be that Se improved mice antioxidant ability, inhibited reproductive cell apoptosis, and increased the decrease of BTB integrity-related genes caused by ZEN.

Proanthocyanidins Attenuation of Chronic Lead-Induced Liver Oxidative Damage in Kunming Mice via the Nrf2/ARE Pathway.

Lead is harmful for human health and animals. Proanthocyanidins (PCs), a natural antioxidant, possess a broad spectrum of pharmacological and medicinal properties. However, its protective effects against lead-induced liver damage have not been clarified. This study was aimed to evaluate the protective effect of PCs on the hepatotoxicity of male Kunming mice induced by chronic lead exposure. A total of 70 healthy male Kunming mice were averagely divided into four groups: control group, i.e., the group exposed to lead, the group treated with PCs, and the group co-treated with lead and PCs. The mice exposed to lead were given water containing 0.2% lead acetate. Mice treated in the PCs and PCs lead co-treated groups were given PC (100 mg/kg) in 0.9% saline by oral gavage. Lead exposure caused a significant elevation in the liver function parameters, lead level, lipid peroxidation, and inhibition of antioxidant enzyme activities. The induction of oxidative stress and histological alterations in the liver were minimized by co-treatment with PCs. Meanwhile, the number of Transferase-Mediated Deoxyuridine Triphosphate-Biotin Nick End Labeling (TUNEL)-positive cells was significantly reduced in the PCs/lead co-treated group compared to the lead group. In addition, the lead group showed an increase in the expression level of Bax, while the expression of Bcl-2 was decreased. Furthermore, the lead group showed an increase in the expression level of endoplasmic reticulum (ER) stress-related genes and protein (GRP78 and CHOP). Co-treated with PCs significantly reversed these expressions in the liver. PCs were, therefore, demonstrated to have protective, antioxidant, and anti-ER stress and anti-apoptotic activities in liver damage caused by chronic lead exposure in the Kunming mouse. This may be due to the ability of PCs to enhance the ability of liver tissue to protect against oxidative stress via the Nrf2/ARE signaling pathway, resulting in decreasing ER stress and apoptosis of liver tissue.

[Emodin alleviates pulmonary fibrosis through inactivation of TGF-ß1/ADAMTS-1 signaling pathway in rats].

Objective To explore the role of transforming growth factor-ß1 (TGF-ß1)/a disintegrin-like and metalloproteinase with thrombospondin type 1 motif (ADAMTS-1) signaling pathway in emodin's anti-pulmonary fibrosis. Methods Sixty SD rats were randomly divided into 6 groups: normal control group, sham-operated group, model group, low-dose emodin intervention group (20 mg/kg), high-dose emodin intervention group (80 mg/kg) and prednisone group (5 mg/kg). Each group included 10 animals. Rats in the latter 4 groups were intratracheally injected with bleomycin A5 to induce pulmonary fibrosis, whereas bleomycin A5 was replaced by normal saline in sham-operated group. From the second day, rats in the low- and high-dose emodin intervention groups were intragastrically treated with 2 mL of 20 and 80 mg/kg emodin, respectively. Rats in the prednisone group were intragastrically administrated with 2 mL of 5 mg/kg prednisone acetate. However, rats in the normal control and sham-operated and model groups were treated with 2 mL of normal saline. All rats were sacrificed on day 28 after modeling. Subsequently, blood and pulmonary tissue specimen were taken. The pathological changes of pulmonary tissues were observed using routine HE and Masson staining. The expressions of TGF-ß1, ADAMTS-1, collagen type 1 (Col1) and Col3 in pulmonary tissues were measured by quantitative real-time PCR and Western blotting. Serum levels of procollagen type 1 carboxy terminal propeptide (P1CP) and procollagen type 3 aminoterminal propeptide (P3NP) were detected by ELISA. Results Compare with the model group, the alveolitis and pulmonary fibrosis extent in each drug-treated group were significantly alleviated. In comparison with normal control group or sham-operated group, the mRNA and protein levels of TGF-ß1, Col1 and Col3 in pulmonary tissues and the serum levels of P1CP and P3NP increased, but the mRNA and protein levels of ADAMTS-1 decreased in model group. After treatment with low- and high-dose emodin or prednisone, the mRNA and protein levels of TGF-ß1, Col1 and Col3 in pulmonary tissues and the serum levels of P1CP and P3NP were significantly downregulated, while the mRNA and protein levels of ADAMTS-1 in pulmonary tissues were significantly upregulated as compared with the model group. Moreover, In comparison with the low-dose emodin intervention group, the above indicators were significantly improved in the high-dose emodin intervention or prednisone group. However, the above indicators were not significantly different between the high-dose emodin intervention group and the prednisone group. Conclusion Increased degradation of Col1 and Col3 in pulmonary tissues due to the inactivation of TGF-ß1/ADAMTS-1 signaling pathway may be a significant mechanism by which emodin protects rats against pulmonary fibrosis.

The Influence of Selenium Yeast on Hematological, Biochemical and Reproductive Hormone Level Changes in Kunming Mice Following Acute Exposure to Zearalenone.

Healthy male Kunming mice received selenium yeast for 14 days prior to a single oral administration of zearalenone (ZEN). After 48 h, blood samples were collected for analysis and showed that mice in the ZEN-treated group has significantly decreased lymphocytes (P < 0.05) and platelets (P < 0.05) along with an increased white blood cell (WBC) count and other constituents (P < 0.05). The serum biochemistry analysis of the ZEN group indicated that glutamic pyruvic transaminase (ALT), glutamic oxaloacetic transaminase (AST), urea, and uric acid were significantly increased (P < 0.05), whilst total bilirubin (TB) and albumin (ALB) were decreased along with serum testosterone and estrogen (P < 0. 05). The level of malondialdehyde (MDA) in the serum of the ZEN group was significantly increased whilst glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) had significantly decreased (P < 0.05). Treatment with selenium yeast had a significant effect on response with most of the experimental parameters returning to levels similar to those observed in the untreated control mice. From these data, it can be concluded that ZEN is highly poisonous in Kunming mice with high levels of toxicity on the blood, liver, and kidneys. High levels of oxidative stress were observed in mice and pre-treatment with selenium yeast by oral gavage is effective in the ameliorated effects of ZEN-induced damage.

The Protective Effect of Grape-Seed Proanthocyanidin Extract on Oxidative Damage Induced by Zearalenone in Kunming Mice Liver.

Although grape-seed proanthocyanidin extract (GSPE) demonstrates strong anti-oxidant activity, little research has been done to clearly reveal the protective effects on the hepatotoxicity caused by zearalenone (ZEN). This study is to explore the protective effect of GSPE on ZEN-induced oxidative damage of liver in Kunming mice and the possible protective molecular mechanism of GSPE. The results indicated that GSPE could greatly reduce the ZEN-induced increase of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. GSPE also significantly decreased the content of MDA but enhanced the activities of antioxidant enzymes SOD and GSH-Px. The analysis indicated that ZEN decreased both mRNA expression levels and protein expression levels of nuclear erythroid2-related factor2 (Nrf2). Nrf2 is considered to be an essential antioxidative transcription factor, as downstream GSH-Px, γ-glutamyl cysteine synthetase (γ-GCS), hemeoxygenase-1 (HO-1), and quinone oxidoreductase 1 (NQO1) decreased simultaneously, whereas the pre-administration of GSPE groups was shown to elevate these expressions. The results indicated that GSPE exerted a protective effect on ZEN-induced hepatic injury and the mechanism might be related to the activation of the Nrf2/ARE signaling pathway.

Intervention of Grape Seed Proanthocyanidin Extract on the Subchronic Immune Injury in Mice Induced by Aflatoxin B1.

The aim was to investigate the prevention of grape seed proanthocyanidin extract (GSPE) on the subchronic immune injury induced by aflatoxin B1 (AFB1) and the possible ameliorating effect of GSPE in mice. The subchronic AFB1-induced immune injury mice model was set up with the continuous administration of 100 µg/kg body weight (BW) AFB1 for six weeks by intragastric administration. Then, intervention with different doses (50 and 100 mg/kg BW) of GSPE was conducted on mice to analyze the changes of body weight, immune organ index, antioxidant capability of spleen, serum immunoglobulin content, and the expression levels of inflammatory cytokines. The prevention of GSPE on the immune injury induced by AFB1 was studied. The GSPE could relieve the AFB1-induced reduction of body weight gain and the atrophy of the immune organ. The malondialdehyde (MDA) level of the spleen in the AFB1 model group significantly increased, but levels of catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-P(X)), and superoxide dismutase (SOD) significantly decreased. The GSPE could significantly inhibit the oxidative stress injury of the spleen induced by AFB1. AFB1 exposure could not significantly change the contents of IgA, IgG, or IgM. AFB1 significantly improved the expression of interleukin 1ß (IL-1ß), IL-6, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ). Additionally, GSPE could decrease the expression of these four proinflammatory factors to different degrees and inhibit the inflammatory reaction of mice. The results suggest that GSPE alleviates AFB1-induced oxidative stress and significantly improves the immune injury of mice induced by AFB1.

[Unsaturated fatty acid of Actinidia chinesis Planch seed oil enhances the antioxidative stress ability of rats with pulmonary fibrosis through activating Keap 1/Nrf 2 signaling pathway].

OBJECTIVE: To observe the effects of unsaturated fatty acid of Actinidia chinesis Planch(USFA-ACP) seed oil on bleomycin-induced pulmonary fibrosis in rats, and to explore whether the effect is mediated by Kelch-like ECH-associated protein 1 (Keap 1)/nuclear factor-erythroid 2-related factor 2 (Nrf 2)signaling pathway. METHODS: Sixty SD rats were randomly divided into control group, model group, (60, 120, 180) mg/kg USFA-ACP seed oil treatment group and 5 mg/kg prednisone group. Each group included 10 animals. Rats in the control group were intratracheally administered with normal saline, and the rest of five groups were intratracheally administered with bleomycin A5 to establish pulmonary fibrosis models. From the second day, rats in the three USFA-ACP seed oil treatment groups were intragastrically treated with 60, 120 and 180 mg/kg USFA-ACP seed oil correspondingly. The prednisone group were intragastrically administrated with 5 mg/kg prednisone acetate. Control and model groups were treated with normal saline. All rats were sacrificed on day 28. Pulmonary tissues were then removed, and HE and Masson staining were performed. The contents of hydroxyproline (HYP), reactive oxygen species(ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione-peroxidase (GSH-Px) in pulmonary tissue homogenates were measured through the commercial kits. The protein expressions of Keap 1 and Nrf2 in pulmonary tissues were analyzed using Western blotting. RESULTS: Compared with the model group, the alveolitis and pulmonary fibrosis extent in 60, 120, 180 mg/kg USFA-ACP seed oil treatment groups as well as the prednisone group were significantly alleviated, HYP, ROS and MDA contents in pulmonary tissues, Keap 1 protein expression in the cytoplasm decreased remarkably, while SOD, CAT and GSH-Px contents in pulmonary tissues, Nrf2 protein expression in the nucleus increased. Moreover, compared with 60 mg/kg USFA-ACP seed oil treatment group, the above indicators were significantly improved in 120 and 180 mg/kg USFA-ACP seed oil treatment group and prednisone group. However, there was no significant difference between 120 and 180 mg/kg USFA-ACP seed oil treatment groups and prednisone group. CONCLUSION: USFA-ACP seed oil can inhibit pulmonary fibrosis in rats, and the mechanism may be associated with the activation of the Keap1/Nrf 2 signaling pathway to increase the production of antioxidases in the pulmonary tissues.

Ovarian toxicity induced by dietary cadmium in hen.

To investigate the toxicity of cadmium (Cd) on female reproduction in birds, this study was conducted to determine the changes in biochemical parameters of serum and ovary tissue caused by dietary cadmium in hens. Ninety 50-day-old hyline white hens were randomly divided into three groups (30 hens per group): a control group was fed with basal diet, a low dose group was fed with basal diet containing 140 mg/kg CdCl(2) and a high dose group was fed with basal diet containing 210 mg/kg CdCl2. After being treated with Cd for 20, 40 and 60 days, ovary and serum samples were collected and examined for Cd content, histological evaluations, malondialdehyde (MDA) content, glutathione peroxidase (GPx) content, activities of superoxide dismutase (SOD), nitric oxide (NO) content, nitric oxide synthase (NOS) activity, and serum estradiol and progestogen levels. The results showed that the content of Cd, MDA, NO and the activity of NOS in ovary and serum were increased (P < 0.05), while the level of GPx and the activity of SOD were decreased (P < 0.05) in low dose and high dose groups. A time- and dose-dependent correlation was observed between serum and ovary tissue cadmium levels. The number of apoptotic cells in the ovary was increased in the Cd treatment group (P < 0.05). Extensive damage was observed in the ovary. The level of estradiol and progestogen in the serum of low dose and high dose groups was decreased significantly (P < 0.05). It indicated that Cd exposure resulted in oxidative damage of hens' ovary tissue by altering antioxidant defense enzyme systems, lipid peroxidation, apoptosis and endocrine disturbance which may be possible underlying reproductive toxicity mechanisms induced by Cd.