Superoxide Dismutase mRNA Expression Research Articles

Dietary supplementation of ornithine improved the growth, immune response and acute NH3 stress tolerance of Pacific white shrimp, Penaeus vannamei

Ornithine is an arginine family amino acid and is not incorporated into protein. This study evaluated its role in growth, immune response and acute NH3 stress tolerance of Penaeus vannamei. Six diets with graded levels (0.6, 0.9, 1.2, 1.5, 1.8, 2.1gkg-1) of L-ornithine were formulated, and fed the shrimp for 8 weeks. The growth of shrimp was significantly improved with the dietary ornithine levels increased from 0.6 to 1.5gkg-1. Feed efficiency, protein efficiency ratio and protein productive value showed a similar trend to the growth performance of shrimp. Whole body protein and muscle lipid of shrimp were significantly increased in shrimp fed 1.8gkg-1 ornithine compared to those fed 0.6gkg-1 ornithine. The contents of several amino acids were increased with the dietary ornithine increased to 1.5gkg-1. Elevated levels of ornithine increased the Nitric Oxide (NO) content and suppressed arginase activity in the hemolymph. The relative mRNA expression of superoxide dismutase, heat shock protein 70, dorsal and caspase 3 were increased with the dietary addition of ornithine, while the mRNA level of arginase was decreased with the increasing dietary ornithine levels. After 9h acute NH3 stress, mortality of shrimp reduced with the increasing dietary ornithine levels. The relative mRNA levels of superoxide dismutase, heat shock protein 70, dorsal and catalase were increased with the dietary addition of ornithine after the acute NH3 stress. The second-order regression analysis of weight gain and survival after acute stress revealed that the suitable ornithine content in the shrimp diet was 1.4-1.5gkg-1.

Erjingwan and Alzheimer's disease: research based on network pharmacology and experimental confirmation.

Alzheimer's disease (AD), a challenging neurodegenerative condition, has emerged as a significant global public health concern. The Chinese medicine decoction Erjingwan (EJW) has shown promising efficacy in AD treatment, though its mechanism remains unclear. This study aims to elucidate the mechanism by which EJW treats AD through network pharmacology analysis and in vivo experiments. We identified EJW's components using the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database and determined AD-related targets from various databases. A network comprising herbs-compounds-targets was established, and EJW's core targets were ascertained through protein-protein interaction (PPI) analysis. This study assessed the cognitive abilities of APP/PS1 mice using Morris water mazes and Y mazes, in addition to analyzing blood samples for triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) levels. Brain tissues were examined histologically with HE staining, Nissl staining, and immunohistochemistry (IHC) for amyloid β-protein (Aβ) detection. Superoxide dismutase (SOD), reactive oxygen species (ROS), Interleukin-1β (IL-1β), and Interleukin-6 (IL-6) levels in the hippocampal region were measured by ELISA. mRNA expression of apolipoprotein A-I (APOA-I), apolipoprotein B (APOB), apolipoprotein E4 (APOE4), advanced glycation end products (AGE), the receptor for AGE (RAGE), and nuclear factor kappa-B (NF-κB) was evaluated by quantitative PCR (q-PCR). Western blotting was used to detect the expression of AGE, RAGE, NF-κB, and Tau protein. Screening identified 57 chemical components and 222 potential targets of EJW. Ten core targets for AD treatment were identified, with enrichment analysis suggesting EJW's effects are related to lipid metabolism and AGEs/RAGE pathways. EJW enhanced learning and memory in APP/PS1 mice, protected neuronal structure in the hippocampal region, reduced Aβ deposition, and altered levels of TG, TC, LDL, IL-1β, and IL-6, and the expression of APOE4, AGEs, RAGE, NF-κB, and Tau protein, while increasing SOD, APOA-I, and APOB mRNA expression. The study identified four core components of EJW-iosgenin, baicalein, beta-sitosterol, quercetin-and ten core targets including AKT1, IL6, VEGFA, TP53, CASP3, for treating AD. Experimental results demonstrate EJW's capacity to modulate lipid profiles, reduce pathological markers such as Aβ1-42, Tau, IL-6, IL-1β, reactive oxygen species, SOD, and enhance cognitive functions in APP/PS1 mice, potentially through inhibiting the AGEs/RAGE/NF-κB pathway.

Effect of in-ovo inoculation of betaine on hatchability, serum antioxidant levels, muscle gene expression and intestinal development of broiler chicks.

This study investigated the effects of in-ovo inoculation of betaine on hatchability, hatching weight, and intestinal development, as well as serum and expression levels of some antioxidants in the posthatched chicks. A total of 350 fertile eggs of Hubbard efficiency plus breeder's flock were incubated at normal incubation temperature (37.5°C) and randomly assembled into 3 groups with 4 replicates, and 25 eggs per each. The experimental groups were allocated as noninjected control group (CN), diluent-injected group (CP, 0.1 mL saline), and betaine-injected group (B, 2.5 mg in 0.1 mL saline). The injections were performed in the air cells of the eggs on the 12th day of the embryonic phase. Hatchability percentage, hatching weight, serum-reduced glutathione (GSH), and superoxide dismutase (SOD) were estimated in 7-day-old chicks. Moreover, expression levels of the nuclear factor erythroid 2-related factor 2 (Nrf2) and SOD were determined in the breast skeletal muscles of chicks. Jejunum histo-morphometric analysis was assessed with computerised morphometric measurements. The results revealed that the hatchability percentage was not influenced by in-ovo injection of betaine or vehicle while betaine significantly increased the hatchling's weight of chicks. Moreover, there were a significant increase in SOD and Nrf2 mRNA expression levels. In-ovo injection of betaine significantly induced positive effects on intestinal morphometry by ameliorating the jejunal villus length, the ratio of villus height to villus width, and absorptive surface area.

Effects of Perilla frutescens Var. Acuta in Busulfan-Induced Spermatogenesis Dysfunction Mouse Model.

The leaves of Perilla frutescens var. acuta (PFA) are generally reported to have antioxidant, anti-allergic, anti-inflammatory, and antitumor effects and commonly used as a traditional medicine in East Asia. This study aimed to investigate the protective effect and antioxidant activity of PFA on busulfan-induced testicular dysfunction, histological damage, oxidative stress (OS), sperm quality, and hormone levels using a mouse model. C57BL/6 male mice were divided into four groups: control, busulfan-only treated, and varying concentrations of PFA (100 and 200 mg/kg) with busulfan. In the busulfan group, 40 mg/kg of busulfan was intraperitoneally injected to induce azoospermia. Mice were orally administered PFA for 35 consecutive days after busulfan administration. Samples were collected and assessed for testis/body weight, testicular histopathology, sperm quality, serum hormone levels, and OS to evaluate the effects of PFA treatment on spermatogenesis dysfunction induced by busulfan. The busulfan-induced testicular dysfunction model showed reduced testis weight, adverse histological changes, significantly decreased sex hormones and sperm quality, and attenuated OS. These results indicate that PFA treatment significantly increased testis weight, testis/body weight, epididymal sperm count, motility, and testosterone level compared with busulfan alone. PFA treatment also attenuated the busulfan-induced histological changes. Furthermore, compared with mice treated with busulfan alone, PFA supplementation upregulated the testicular mRNA expression of the antioxidant enzymes superoxide dismutase 1 (Sod1) and glutathione peroxidase 1 (Gpx1), with a decrease in malondialdehyde (MDA) production and an increase in SOD and GPx activities. This study shows that PFA exerts a protective effect against testicular damage by attenuating OS induced by busulfan. Our results suggest that PFA is a potentially relevant drug used to decrease the side effects induced by busulfan on testicular function and sperm during cancer chemotherapy.

Pro-oxidation status of rotator cuff tissue and expression of Beclin-1 and mTOR in patients with rotator cuff injury

To explore pro-oxidative state of rotator cuff tissue and expression levels of Beclin-1 and mam-malian target of rapamycin(mTOR) in patients with acute and chronic rotator cuff injury, and then analyzed relationship between rotator cuff injury and oxidative stress and autophagy. Forty patients with rotator cuff injury were seleceted from July 2019 to December 2020, and divided into male chronic injury group, male acute injury group, female chronic injury group, and female acute injury group, 10 patients in each group. All patients were performed rotator cuff repair under arthroscopy. The sample of tendon at the rotator cuff injury site of the patient was taken during operation, and total reactive oxygen species (ROS) and superoxide dismutase(SOD) were detected by detection kit;expression of Beclin-1 and mTOR mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR), and Western-blot was applied to detect protein expression of Beclin-1 and p-mTOR/mTOR. There were no significant difference in expression of ROS, SOD, Beclin-1mRNA and mTOR mRNA between male and female chronic injury groups, and between male and female acute injury groups (P>0.05); ROS, SOD and Beclin-1mRNA in male chronic injury group were higher than those in male chronic injury group, while mTOR mRNAand protein decreased (P<0.05);ROS, SOD and Beclin-1 mRNA in female chronic injury group were up-regulated compared with female acute injury group, while mTOR mRNA was down-regulated (P<0.05). Chronic rotator cuff injury is more likely to stimulate the pro-oxidation state of rotator cuff tissue than acute rotator cuff injury, which could up-regulating expression of autophagy factor Beclin-1 and down-regulating expression of mTOR. Therefore, patients with chronic rotator cuff injury may have higher levels of oxidative stress and autophagy.

PSV-8 Maternal Live Yeast Supplementation Improved Gut Health in Suckling and Weaned Piglets

Abstract Recent studies have highlighted the importance of maternal nutritional intervention in modulating the gastrointestinal development and health of offspring. The objective of this study was to determine the effects of live yeast supplementation to sows during late gestation and lactation periods on the gut health of piglets pre-weaning and immediately post-weaning. Based on parity and expected farrowing dates, on d 77 of gestation, 40 sows were allotted to 2 dietary treatments: without (CON) or with (LY) live yeast supplementation at 0.05% of diet during gestation and 0.1% during lactation. On postnatal days (PND) 0, 10, 18, and post-weaning days (PWD) 7 and 14, one piglet from 10 sows per treatment was selected for intestinal tissue collection (n = 10). Results showed that maternal LY supplementation increased mRNA expression of interleukin (IL)-6 on PND 18 and IL-1β on PWD 14 in the ileal mucosa (P &amp;lt; 0.05), with a tendency for greater IL-10 on PND 18 (P = 0.08). Additionally, LY piglets had increased mRNA expression of superoxide dismutase 1 on PND 10, 18, and PWD 14 (P &amp;lt; 0.05) and tended to have a greater mRNA abundance of catalase on PND 14 in the ileal mucosa (P = 0.09). Compared with CON piglets, LY piglets had an increased protein abundance of E-cadherin on PND 0, PWD 7, and 14 in the jejunal mucosa (P &amp;lt; 0.05). The LY piglets also had a greater protein abundance of occludin and claudin-4 in the jejunal mucosa on PWD 14 (P &amp;lt; 0.05). However, no differences were found for jejunal histomorphological measurements between treatments (P &amp;gt; 0.05). In conclusion, maternal LY supplementation may have a long-term protective effect on gut health of offspring by regulating the expression of tight junction proteins, inflammatory response, and antioxidant capacity.

Biochemical and gene expression alterations due to individual exposure of atrazine, dichlorvos, and imidacloprid and their combination in zebrafish.

In environmental toxicology, combined toxicity has emerged as an important concern. Atrazine (ATZ), dichlorvos (DIC), and imidacloprid (IMD) are the major pesticides, extensively used to control insect, flies, mosquitoes, and weed. Here, we investigate whether the exposure to three different types of pesticides individually and in combination for 24h alters antioxidant enzyme responses in zebrafish (Danio rerio). Oxidative stress parameters (biochemical and mRNA expression), acetylcholinesterase (AChE) activity, and Metallothionein-II (MT-II) mRNA expression levels were measured. Present work includes toxicological assessment of individual and combined (CMD) exposure of ATZ (185.4µM), DIC (181µM), IMD (97.8 µ), and CMD (ATZ 92.7µM + DIC 90.5µM + IMD 48.9µM), in the liver, kidney, and brain of adult zebrafish. Lipid peroxidation (LPO), glutathione (GSH) content, AChE, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity along with mRNA expression of SOD, CAT, GPx, and MT-II were evaluated. Briefly, LPO, GSH content, the activity of AChE, and all antioxidant enzymes enhanced significantly in individual exposure, which was further altered in the CMD group. The mRNA expression of SOD, CAT, GPx, and MT-II in the liver and kidney showed significant down-regulation in all exposed groups. In the brain, significant upregulation in mRNA expression of SOD, CAT, GPx, and MT-II was observed in DIC and IMD groups, while ATZ and CMD showed significant downregulation except for GPx. Findings postulate that the CMD group exhibits synergistic toxic manifestation. The present study provides the baseline data on the combined toxic effects of pesticides and suggests regulating the use of pesticides.

Effects of microfiber and bead microplastic exposure in the goldfish Carassius auratus: Bioaccumulation, antioxidant responses, and cell damage

We confirmed antioxidant-related gene expression, bioaccumulation, and cell damage following exposure to various microplastics in vivo and in vitro in the goldfish Carassius auratus. Exposure of C. auratus to a 500 µm fiber-type microplastic environment (MF; 10 and 100 fibers/L) and two sizes (0.2 and 1.0 µm) of beads (MB; 10 and 100 beads/L) for 120 h increased superoxide dismutase (SOD) mRNA expression in the liver until 24 h followed by a decrease. Whereas, catalase (CAT) mRNA expression increased from 12 h to the end of the in vivo experiment. In vitro experiments were conducted with diluted microfibers (1 and 5 fibers/L) and microbeads (1 and 5 beads/L) using cultured liver cells. The results of SOD and CAT mRNA expression analysis conducted in vitro showed a tendency similar to those of experiments conducted in vivo. The H2O2 level increased in the high-concentration experimental groups compared with that in the low-concentration groups of 0.2-µm beads. In addition, the H2O2 level increased in both MF and MB groups from 12 h of exposure. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in plasma were used as indicators of liver damage in fish. The ALT and AST levels increased up to 120 h after exposure. Caspase-3 (casp-3) mRNA expression was higher in the MB group than in the MF group. We visually confirmed liver casp-3 mRNA signals using in situ hybridization. The degree of DNA damage in the MF and MB high-concentration groups increased with the exposure time. The tail length and percent of DNA in the tail of the MB group were significantly higher than those of the MF group, confirming that DNA damage was greater in the MB group. Both fiber- and bead-type microplastics induced oxidative stress in C. auratus, but the bead-type induced greater stress than the fiber-type.

Dietary supplementation with 2-hydroxy-4-methyl(thio) butanoic acid and DL-methionine improves productive performance, egg quality and redox status of commercial laying ducks.

This experiment aimed to study the effects of supplemental methionine sources, 2-hydroxy-4 methyl(thio) butanoic acid (HMTBa) and DL-Methionine (DL-Met), on productive performance, egg quality, and redox status of laying ducks. A total of 792 healthy 25-wk-old Longyan laying ducks with similar body weights were randomly allotted to 11 treatment groups. Each treatment group had 6 replicates of 12 ducks. The trial lasted for 16wk. Ducks were fed a basal deficient diet (Met: 0.24%; Met+Cys: 0.51%) or supplemented with DL-Met or HMTBa at 0.05%, 0.12%, 0.19%, 0.26%, and 0.33% of diet, respectively. Compared with the basal diet, supplementation with either DL-Met or HMTBa increased the average egg weight, egg mass, and decreased feed to egg ratio during the whole trial period (P<0.05). Albumen weight and its ratio to total egg weight were increased, but yolk and shell ratio, albumen height, Haugh unit and shell breaking strength were decreased (P<0.05). Dietary DL-Met or HMTBa supplementation increased taurine, methionine, leucine, tryptophan and arginine content, and decreased serine and lysine content in plasma (P<0.05). The redox status of laying ducks was improved by enhancing the glutathione peroxidase and catalase activities, glutathione content and its ratio relative to glutathione (oxidized) content and decreasing malondialdehyde content and increasing mRNA expression of superoxide dismutase-1, glutathione peroxidase-1, hemeoxygenase-1 and nuclear factor-like 2 in liver and ileum with the supplementation of DL-Met or HMTBa (P<0.05). Liver health status measured by average area proportion lipid droplet was improved with supplementation of DL-Met or HMTBa (P<0.05). Villus height and villus height to crypt depth ratio in the ileum and the ileal gene expression of tight junction protein and occludin were increased with DL-Met or HMTBa supplementation (P<0.05). Taken together, these results suggested that the efficacy of dietary supplementation of HMTBa was similar to DL-Met, and it ranged from 98% to 100% for productive performance and egg albumen ratio in laying ducks (25 to 41wk).

Toxicological effects of meloxicam on physiological and antioxidant status of common carp (Cyprinus carpio).

Fish in aquatic environments are end consumers of the food chain and are widely used for the evolution effects of environmental pollution and their interactions in aquatic ecosystem. In the present study, common carp (Cyprinus carpio) fingerlings were selected to assess the potential risk and aquatic toxicity of meloxicam as a non-steroidal anti-inflammatory and a commonly used pharmaceutical drug. In order to evaluate meloxicam toxicological effect on haematological, antioxidant status, enzymological and histological parameters, based on its LC50 24h acute toxicity (10.05mgL-1 ), fish fingerlings were exposed to four doses of meloxicam including; 0 (control), 0.1 (low), 1 (medium) and 2mgL-1 (high) under static bioassay method for 28 days. The results showed that sublethal doses of meloxicam significantly decreased alanine aminotransferase, alkaline phosphatase, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) levels in comparison with the control group after 28 days (p<0.05). However, red blood cell, haematocrit, haemoglobin and malondialdehyde values in fish exposed to meloxicam significantly increased alongside its concentration (p<0.05) more than the control group after 28 days. SOD, CAT and GPX mRNA expression levels in gill, liver, kidney and brain organ of fish under meloxicam treatment were significantly down-regulated compared to the control group (p<0.05). Histopathological assessment showed the increased vacuolation in hepatocytes in liver of fish exposure to medium and high doses of meloxicam. In conclusion, meloxicam induces oxidative stress in common carp which results a disruption of physiological and health status of this species based on our current findings.

NDUFC2 deficiency exacerbates endothelial mesenchymal transformation during ischemia-reperfusion via NLRP3.

Ischemic stroke is the main type of cerebrovascular disease. Emergency thrombectomy combined with medication therapy is currently the primary treatment for stroke. Inflammation and oxidative stress induced by ischemia-reperfusion cause secondary damage to blood vessels, especially endothelial mesenchymal transformation (EndoMT). However, much is still unclear about the role of EndoMT in ischemia-reperfusion. In this study, an in vivo ischemia-reperfusion model was established by transient middle cerebral artery occlusion (tMCAO) in wild-type (WT) C57BL/6 mice and NLRP3 (NOD-like receptor thermal protein domain associated protein 3) knockout (KO) C57BL/6 mice. An in vitro ischemia-reperfusion model was established by oxygen glucose deprivation and reoxygenation (OGD/R) of human brain microvascular endothelial cells (HBMECs). α-SMA (alpha smooth muscle actin), CD31 (platelet endothelial cell adhesion molecule-1, PECAM-1/CD31), NDUFC2 (NADH: ubiquinone oxidoreductase subunit C2), and NLRP3 were used to evaluate EndoMT and inflammation. Real-time PCR measured superoxide dismutase 1 (SOD1) and catalase (CAT) mRNA expression to evaluate oxidative stress levels. NLRP3 was activated by ischemia-reperfusion injury and NLRP3 inactivation inhibited the EndoMT in tMCAO mice. Further experiments demonstrated that OGD/R treatment induced NLRP3 activation and EndoMT in HBMECs, which resulted in NDUFC2 deficiency. NDUFC2 overexpression suppressed NLRP3 activation and EndoMT in HBMECs induced by OGD/R. Moreover, NDUFC2 overexpression rescued SOD1 and CAT mRNA expression. These results demonstrated that NDUFC2 deficiency decreased the antioxidant levels, leading to NLRP3 activation and EndoMT during ischemia-reperfusion injury and suggesting that NDUFC2 is a potential drug target for the treatment of ischemic stroke.

Moringa oleifera Leaves Extract Ameliorates Doxorubicin-Induced Cardiotoxicity via Its Mitochondrial Biogenesis Modulatory Activity in Rats.

Doxorubicin, an anthracycline class of anticancer, is an effective chemotherapeutic agent with serious adverse effects, mainly cardiotoxicity. Several possible causes of doxorubicin cardiotoxicity are increased oxidative stress, nucleic acid and protein synthesis inhibition, cardiomyocyte apoptosis, and mitochondrial biogenesis disruptions. Moringa oleifera (MO), a naturally derived medicine, is known for its antioxidative properties and activity in alleviating mitochondrial dysfunction. To determine the potency and possible cardioprotective mechanism of MO leaves aqueous extract via the mitochondrial biogenesis pathway in doxorubicin-induced rats. Twenty-four Sprague-Dawley rats were divided into four groups of six. The first group was normal rats; the second group was treated with doxorubicin 4 mg/kg BW intraperitoneally once weekly for four weeks; the third and fourth groups were treated with doxorubicin 4 mg/kg BW intraperitoneally once weekly, and MO leaves extract at 200 mg/kg BW or 400 mg/kg BW orally daily, for four weeks. At the end of the fourth week, blood and cardiac tissues were obtained and analyzed for cardiac biomarkers, mitochondrial DNA copy number, mRNA expressions of peroxisome-activated receptor-gamma coactivator-1 alpha (PGC-1α), the nuclear factor erythroid 2-related factor 2 (Nrf2), superoxide dismutase 2 (SOD2), caspase 3, the activity of glutathione peroxidase (GPx), levels of 8-hydroxy-2-deoxyguanosine (8-OH-dG), and malondialdehyde. MO leaves extract was shown to decrease biomarkers of cardiac damage (LDH and CK-MB), malondialdehyde levels, and GPx activity. These changes align with the reduction of mRNA expressions of caspase-3, the increase of mRNA expressions of PGC-1αand Nrf2, and the elevation of mitochondrial DNA copy number.MOleaves extracts did not influence the mRNA expressions of superoxide dismutase 2 (SOD2) or the levels of 8-OH-dG. Moringa oleifera leaves extract ameliorates doxorubicin-induced cardiotoxicity by reducing apoptosis and restoring gene expression of PGC-1α and Nrf2, a key regulator in mitochondrial biogenesis.

Mitochondrial dysfunction and cardiac ischemia/reperfusion injury are attenuated by nandrolone: Role of JAK-STAT3 pathway

AimTo investigate the effect of acute treatment with the anabolic steroid (AS) nandrolone decanoate in mitochondrial homeostasis and JAK-STAT3 signaling during the progression of cardiac ischemia/reperfusion injury (IR). MethodsMale Wistar rats (2 months old) were randomly allocated into four experimental groups: Control (CTRL), IR, AS, and AS + AG490. All animals were euthanized 3 days after a single intramuscular injection of nandrolone at 10 mg/kg (AS and AS + AG490 groups) or vehicle (CTRL and IR groups). Baseline mRNA expression of antioxidant enzymes superoxide dismutase (SOD) 1 and 2, glutathione peroxidase, catalase, and myosin heavy chain (MHC) α and β were compared between CTRL and AS groups. Isolated hearts were submitted to ex vivo ischemia and reperfusion, except for hearts from the CTRL group. Before the IR protocol, the JAK-STAT3 inhibitor AG490 was perfused in hearts from the AS + AG490 group. Heart samples were collected during reperfusion to investigate the effects on mitochondrial function.ResultsAntioxidant enzyme mRNA expression was unaffected, whereas the AS group exhibited decreased β- MHC/α-MHC ratio versus the CTRL group. Compared to the IR group, the AS group exhibited better recovery of post-ischemic left ventricular (LV) end-diastolic pressure and LV-developed pressure levels, while infarct size significantly decreased. Furthermore, mitochondrial production, transmembrane potential, and swelling were improved, whereas ROS formation was decreased versus the IR group. These effects were prevented by the perfusion of JAK-STAT3 inhibitor AG490. ConclusionThese findings suggest that acute nandrolone treatment can provide cardioprotection by recruiting the JAK-STAT3 signaling pathway and mitochondrial preservation.

Dietary Selenium-Rich Lactobacillus plantarum Alleviates Cadmium-Induced Oxidative Stress and Inflammation in Bulatmai barbel Luciobarbus capito

Cadmium (Cd) poses a great threat to the breeding of aquatic economic animals. The present study aimed to explain the antagonistic effects of selenium-enriched Lactobacillus plantarum (SL) on Cd toxicity through the expression of oxidative and inflammatory factors. A total of 225 Bulatmai barbel Luciobarbus capito (L. capito) were divided into 3 groups, namely, the control group, the Cd group (Cd, 0.05 mg·L−1), and the SL + Cd group (Cd, 0.05 mg·L−1; Nano Se, 5 mg·kg−1; L. plantarum, 105 CFU·g−1). The experiment lasted for 28 d, Sampling at 14 and 28 d, respectively. The results showed that Cd exposure caused obvious pathological damage to the liver and kidney, and the serum parameter ALT increased significantly (p &lt; 0.05). In the Cd group, the concentration of Cd in the kidney was significantly increased (p &lt; 0.05), and the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in the kidney and gill were significantly decreased; malonaldehyde (MDA) increased significantly (p &lt; 0.05) Then the mRNA expression levels in the kidney and liver were measured. Cd exposure significantly decreased the mRNA expressions of SOD, CAT, GSH-Px, HO-1, I-κBα, and Nrf2 (p &lt; 0.05). The Cd-treated group showed significantly increased NF-kBp65, TGF-β, IL-8, IL-1, Keap1, and TNF-α expression levels. SL significantly alleviated the changes in the above indicators. The results of this study suggest that SL can trigger the Nrf2 signalling pathway and NF-kB signalling pathway to alleviate Cd toxicity. SL might be a potential drug for the treatment of Cd poisoning.

Supplementation of Schisandrin B in Semen Extender Improves Quality and Oxidation Resistance of Boar Spermatozoa Stored at 4 °C.

During cold storage, boar spermatozoa undergo oxidative stress, which can impair sperm function and fertilizing capacity. The objective of the present study was to assess the effects of Schisandrin B (Sch B) in semen extenders on the quality of boar semen stored at hypothermia. Semen was collected from twelve Duroc boars and diluted in extenders supplemented with different concentrations of Sch B (0 μmol/L, 2.5 μmol/L, 5 μmol/L, 10 μmol/L, 20 μmol/L, and 40 μmol/L). Here, we demonstrated that 10 μmol/L Sch B provided the best effects on motility, plasma membrane integrity, acrosome integrity, sperm normality rate, average movement velocity, wobbility, mitochondrial membrane potential (MMP), and DNA integrity of sperm. The results of Sch B effects on antioxidant factors in boar sperm showed that Sch B significantly elevated the total antioxidant capacity (T-AOC) and markedly decreased the reactive oxygen species (ROS) and malondialdehyde (MDA) content of sperm. The expression of catalase (CAT) and superoxide dismutase (SOD) mRNA was increased, while the expression of glutathione peroxidase (GPx) mRNA demonstrated no change compared to non-treated boar sperm. Compared to the non-treated group, Sch B triggered a decrease in Ca2+/protein kinase A (PKA) and lactic acid content in boar sperm. Similarly, Sch B led to a statistically higher quantitative expression of AWN mRNA and a lower quantitative expression of porcine seminal protein I (PSP-I) and porcine seminal protein II (PSP-II) mRNA. In a further reverse validation test, no significant difference was observed in any of the parameters, including adhesion protein mRNA, calcium content, lactic acid content, PKA, and protein kinase G (PKG) activity after sperm capacitation. In conclusion, the current study indicates the efficient use of Sch B with a 10 μmol/L concentration in the treatment of boar sperm through its anti-apoptosis, antioxidative, and decapacitative mechanisms, suggesting that Sch B is a novel candidate for improving antioxidation and decapacitation factors in sperm in liquid at 4 °C.

Protective effect of Capsosiphon fulvescens on oxidative stress-stimulated neurodegenerative dysfunction of PC12 cells and zebrafish larva models

Reactive oxygen species (ROS) at high concentrations induce oxidative stress, an imbalanced redox state that is a prevalent cause of neurodegenerative disorders. This study aimed to investigate the protective effect of Capsosiphon fulvescens (CF) extract on oxidative stress-induced impairment of cognitive function in models of neurodegenerative diseases. CF was extracted with subcritical water and several solvents and H2O2 (0.25 mM) or aluminum chloride (AlCl3; 25 μM) as an inducer of ROS was treated in PC12 neuronal cells and zebrafish larvae. All statistical analyses were performed using one-way analysis of variance and Dunnett’s test using GraphPad Prism. H2O2 and AlCl3 were found to significantly induce ROS production in PC12 neuronal cells and zebrafish larvae. In addition, they strongly affected intracellular Ca2+ levels, antioxidant enzyme activity, brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) signaling, acetylcholinesterase (AChE) activity, and hallmarks of Alzheimer’s disease. However, treatment of H2O2-induced PC12 cells or AlCl3-induced zebrafish larvae with CF subcritical water extract at 90°C and CF water extract effectively regulated excessive ROS production, intracellular Ca2+ levels, and mRNA expression of superoxide dismutase, glutathione peroxide, glycogen synthase kinase-3 beta, β-amyloid, tau, AChE, BDNF, and TrkB. Our study suggested that CF extracts can be a potential source of nutraceuticals that can improve the impairment of cognitive function and synaptic plasticity by regulating ROS generation in neurodegenerative diseases.

Effects of microfiber exposure on medaka (Oryzias latipes): Oxidative stress, cell damage, and mortality

Fiber-type microplastics are major anthropogenic contaminants of marine environments. They are released mainly during cloth washing and are discharged from wastewater treatment plants into aquatic environments. This study aimed to evaluate whether microfiber exposure causes oxidative stress and cell damage in medaka (Oryzias latipes Temminck and Schlegel 1846). Fish were exposed to one of two different concentrations (500 and 1000 fibers/L) of a polyester-based microfiber (MF) for 21 days, and the degree of cell damage and changes in expression of antioxidant enzymes were investigated. Fish survival decreased with increasing concentrations of MF. The expression levels of superoxide dismutase (SOD) and catalase (CAT) increased in MF-exposed groups compared to those in the control. SOD activity increased compared to the control group, and MF exposure induced a significant increase in both SOD activity and mRNA expression over time. CAT mRNA expression increased from day 10 onwards following exposure. Plasma malondialdehyde content increased significantly on day 7 of exposure in the 1000 fiber/L group and on day 10 in the 500 fiber/L group. Caspase-3 mRNA expression significantly increased until day 10 of exposure. A terminal transferase dUTP nick end labeling assay confirmed increased apoptosis, and a comet assay demonstrated that higher DNA damage occurred in response to increased MF concentration and exposure time. In conclusion, we confirmed that MF exposure affects antioxidant reactions in fish, thus inducing oxidative stress, apoptosis, and DNA damage. In addition, a comprehensive understanding of MF pollution in aquatic systems is urgently required.

Effect of Secretome-Hypoxia Mesenchymal Stem Cells on Regulating SOD and MMP-1 mRNA Expressions in Skin Hyperpigmentation Rats

BACKGROUND: Ultraviolet B (UVB) radiation is the main factor causing hyperpigmentation. MSC secretome contains bioactive soluble molecules such as cytokines and growth factors that can accelerate skin regeneration. However, the molecular role of the secretome in hyperpigmentation is still unclear. AIM: This study aimed to determine the effect of secretome hypoxia mesenchymal stem cells (S-HMSC) gel on the expression of superoxide dismutase (SOD) and matrix metalloproteinases (MMP-1) genes in skin tissue of hyperpigmented rats induced by UVB light exposure. MATERIALS AND METHODS: Experimental research with post-test only control group. The control, base gel, T1 and T2 groups were UVB irradiated 6 times in 14 days at 302 nm with an minimal erythema dose of 390 mJ/cm2, respectively, while sham group did not receive UVB exposure. T1 was given 100 uL of S-HMSC gel and T2 was given 200 uL of S-HMSC gel every day for 14 days, while base gel received base gel. On day 15, skin tissue was isolated and analyzed for SOD and MMP-1 expression using qRT-PCR. RESULTS: The relative expression of the SOD gene in the treatment group (P1 = 0.47 ± 0.20, P2 = 1.22 ± 0.47) increased with increasing dose compared to the control group (UVB = 0.05 ± 0.01, Base gel = 0.05 ± 0.02). The relative expression of the MMP-1 gene in the treatment group (T1 = 5.82 ± 1.16, T2 = 2.86 ± 1.57) decreased with increasing dose compared to the control group (Control = 10.10 ± 2.31, and Base gel = 9.55 ± 1.29). CONCLUSION: Administration of S-HMSC gel can increase SOD gene expression and decrease MMP-1 gene expression in skin tissue of hyperpigmented rats model induced by UVB light.

Effects of bamboo leaf extract on energy metabolism, antioxidant capacity, and biogenesis of small intestine mitochondria in broilers.

The present study was carried out to investigate the effects of bamboo leaf extract (BLE) on energy metabolism, antioxidant capacity, and biogenesis of broilers' small intestine mitochondria. A total of 384 one-day-old male Arbor Acres broiler chicks were randomly divided into four groups with six replicates each for 42 d. The control group was fed a basal diet, whereas the BLE1, BLE2, and BLE3 groups consumed basal diets with 1.0, 2.0, and 4.0 g/kg of BLE, respectively. Some markers of mitochondrial energy metabolism including isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, and malate dehydrogenase and some markers of redox system including total superoxide dismutase, malondialdehyde, and glutathione were measured by commercial colorimetric kits. Mitochondrial and cellular antioxidant genes, mitochondrial biogenesis-related genes, and mitochondrial DNA copy number were measured by quantitative real-time-polymerase chain reaction (qRT-PCR). Data were analyzed using the SPSS 19.0, and differences were considered as significant at P < 0.05. BLE supplementation linearly increased jejunal mitochondrial isocitrate dehydrogenase (P < 0.05) and total superoxide dismutase (P < 0.05) activity. The ileal manganese superoxide dismutase mRNA expression was linearly affected by increased dietary BLE supplementation (P < 0.05). Increasing BLE supplementation linearly increased jejunal sirtuin 1 (P < 0.05) and nuclear respiratory factor 1 (P < 0.05) mRNA expression. Linear (P < 0.05) and quadratic (P < 0.05) responses of the ileal nuclear respiratory factor 2 mRNA expression occurred with increased dietary BLE levels. In conclusion, BLE supplementation was beneficial to the energy metabolism, antioxidant capacity, and biogenesis of small intestine mitochondria in broilers. The dose of 4.0 g/kg BLE demonstrated the best effects.

Modulation of Virulence-Associated Traits in Aspergillus fumigatus by BET Inhibitor JQ1.

Aspergillus fumigatus is a disease-causing, opportunistic fungus that can establish infection due to its capacity to respond to a wide range of environmental conditions. Secreted proteins and metabolites, which play a critical role in fungal-host interactions and pathogenesis, are modulated by epigenetic players, such as bromodomain and extraterminal domain (BET) proteins. In this study, we evaluated the in vitro and in vivo capability of the BET inhibitor JQ1 to modulate the extracellular proteins and virulence of A. fumigatus. The abundance of 25 of the 76 extracellular proteins identified through LC-MS/MS proteomic analysis changed following JQ1 treatment. Among them, a ribonuclease, a chitinase, and a superoxide dismutase were dramatically downregulated. Moreover, the proteomic analysis of A. fumigatus intracellular proteins indicated that Abr2, an intracellular laccase involved in the last step of melanin synthesis, was absent in the JQ1-treated group. To investigate at which level this downregulation occurred and considering the ability of JQ1 to modulate gene expression we checked the level of ABR2, Chitinase, and Superoxide dismutase mRNA expression by qRT-PCR. Finally, the capacity of JQ1 to reduce the virulence of A. fumigatus has been proved using Galleria mellonella larvae, which are an in vivo model to evaluate fungal virulence. Overall, the promising activity exhibited by JQ1 suggests that A. fumigatus is sensitive to BET inhibition and BET proteins may be a viable target for developing antifungal agents.