Antioxidant Improvement Research Articles

Edible Coating for Fresh-Cut Fruit and Vegetable Preservation: Biomaterials, Functional Ingredients, and Joint Non-Thermal Technology.

This paper reviews recent advances in fresh-cut fruit and vegetable preservation from the perspective of biomacromolecule-based edible coating. Biomaterials include proteins, polysaccharides, and their complexes. Compared to a single material, the better preservation effect was presented by complexes. The functional ingredients applied in the edible coating are essential oils/other plant extracts, metals/metal oxides, and organic acids, the purposes of the addition of which are the improvement of antioxidant and antimicrobial activities and/or the mechanical properties of the coating. The application of edible coating with other preservation technologies is an emerging method, mainly including pulsed light, short-wave ultraviolet, modified atmosphere packaging, ozonation, and γ-irradiation. In the future, it is crucial to design coating formulations based on preservation goals and sensory characteristics. The combination of non-thermal preservation technology and edible coating needs to be strengthened in research on food preservation. The application of AI tools for edible coating-based preservation should also be focused on. In conclusion, edible coating-based preservation is promising for the development of fresh-cut fruits and vegetables.

Improvement of antioxidant, emulsification properties and thermal stability of egg white protein by covalent binding to gallic acid/tannic acid and xanthan gum

This study aimed to improve the functional properties of egg white protein (EWP) by covalent modification of EWP with xanthan gum (XG) and gallic acid (GA)/tannic acid (TA) to form covalent complexes. The structure and functional properties of EWP before and after modification were explored. The results showed that the grafting degree of EWP-GA-XG and EWP-TA-XG reached 37.23% and 44.01% respectively measured by the OPA method. The secondary structure of EWP became loose after reaction with GA/TA and XG, with a decrease in the content of α-helix and an increase in the β-sheet content, thus contributing to the improvement of its functional properties. The DPPH and ABTS radical scavenging rate and iron reduction ability of EWP-GA-XG (44.94%, 56.38%, 18.29 mg VC/μmol) and EWP-TA-XG (85.45%, 88.39%, 39.26 mg VC/μmol) complexes were significantly improved compared with EWP (7.90%, 12.94%, 0.12 mg VC/μmol). The emulsion activity index and emulsion stability index of EWP-GA-XG (10.05 m2/g, 96.43%) and EWP-TA-XG (11.04 m2/g, 96.53%) complexes were also improved as compared to those of EWP (5.94 m2/g, 51.45%). Moreover, the peak transition temperatures of EWP-GA-XG (138.09 °C) and EWP-TA-XG (143.96 °C) complexes were higher than that of EWP (125.00 °C). This study may provide the theoretical basis for improving the functional properties of EWP and expanding its application in the field of food.

SNEDDS to improve the bioactivities of Pandanus tectorius leaves: Optimization, antioxidant, and anticancer activities via apoptosis induction in human cervical cancer cell line

Cancer continues to be a deadly disease on a global scale. Furthermore, despite the high expense of their development, synthetic chemotherapeutic drugs currently being used in clinical settings have failed to meet expectations during the past ten years. Therefore, new herbal medications might be alternative anticancer agents that are effective and affordable. Antioxidants in herbs might lessen oxidative stress and prevent carcinogenesis by slowing down and blocking the initiation of cancer cell development. Some researchers have reported that Pandanus tectorius has antioxidant activity. However, the antioxidant and anticancer properties of P. tectorius leave (PTL) in the form of self-nanoemulsifying drug delivery system (SNEDDS), specifically against human cervical cancer cells (HeLa) have not been studied. This study examined the anticancer activity of PTL-SNEDDS via induction of apoptosis on HeLa cells. All three PTL extracts (hexane, ethyl acetate, and methanol) were successfully formulated into SNEDDS formulation and showed improvement in antioxidant and anticancer activity compared to the crude extract. The cells’ morphological characteristics showed that PTL-SNEDDS-treated cells died from both early and late apoptosis. Thus, these findings introduce PTL-SNEDDS as an anticancer agent against human cervical cancer.

Unveiling the effect of molecular weight of vanillic acid grafted chitosan hydrogel films on physical, antioxidant, and antimicrobial properties for application in food packaging

Till now, a wide range of chitosan (CHS)-based food packaging films have been developed. Yet, the role of molecular weight (MW), which is an important physical property of CHS, in determining the physicochemical and biochemical properties of vanillic acid (VA)-grafted CHS hydrogel films synthesized using CHS with different MWs has not been investigated until now. Three kinds of CHS including low, medium, and high MWs were grafted separately with VA through a carbodiimide mediated coupling reaction. No significant difference in water resistance properties was observed with increasing MW of CHS, in contrast to obvious decrease in light transmittance and opacity. The VA-g-CHS hydrogel films exhibited significantly improved light blocking capacity. A significant improvement in antioxidant (~6-fold) and antimicrobial (~1.2-fold) activity was observed after grafting with VA. In contrast, the free radical scavenging and antimicrobial activity decreased with increasing MW of CHS. Most importantly, VA-g-CHS hydrogel films could maintain the freshness of cherry tomatoes for up to 10 days at ~25 °C. However, no significant difference was observed depending on the MW value of CHS. This pioneering work is of great importance in guiding the selection of MW of CHS biomacromolecule to design hydrogel films with desired physicochemical and biochemical properties.

Effect of Adding Okra Powder and Vitamin C or E to the Diet on some Qualitative Characteristics and Oxidation Indices in the Eggs of Lohmann Brown-Lite Hens

The study employed 300 laying hens at 34 weeks of age, divided into 5 treatments with 3 replicates per replication of 20 birds each, to determine the impact of adding okra powder and vitamins C and E to (Brown-Lite Lohman) egg broiler diets on certain qualitative egg features and oxidation indicators. The treatments were: (T1): control treatment without any addition, (T2) 250 mg vitamin C / kg diet, (T3) 200 mg vitamin E / kg diet, (T4) 2 gm okra powder / kg diet, (T5) ) Add 4 gm of okra powder / kg diet. The results indicated that there were no significant differences in the relative weight of shell, white and yolk compared with the control treatment. And the shell thickness was much greater in the addition treatments than in the control. Compared to the control group, the addition treatments recorded a significant decrease in the value of the peroxide number and an increase in the concentration of estrogen in the egg, indicating that okra at 4 g / kg of feed contributed to the improvement in antioxidants in the egg.

Protective effect of hydroxysafflor yellow A on renal ischemia‑-reperfusion injury by targeting the Akt‑Nrf2 axis in mice.

Ischemic/reperfusion (I/R) injury is the primary cause of acute kidney injury (AKI). Hydroxysafflor yellow A (HSYA), a natural compound isolated from Carthamus tinctorius L., has been found to possess anti-inflammatory and antioxidant properties. However, the protective effects and potential mechanism of HSYA on I/R-induced AKI remains unclear. In the present study, the in vitro hypoxia/reoxygenation (H/R) and in vivo renal I/R models were employed to investigate the renal protective effects and molecular mechanisms of HSYA on I/R-induced AKI. The present results indicated that HSYA pretreatment significantly ameliorated renal damage and dysfunction in the I/R injury mice via enhancing the antioxidant capacity and suppressing the oxidative stress injury, inflammatory response, and apoptosis. Mechanistic studies showed that HSYA could upregulate Akt/GSK-3β/Fyn-Nrf2 axis-mediated antioxidant gene expression both in vitro and in vivo. Moreover, HSYA-mediated improvement in antioxidant, anti-inflammatory, and anti-apoptotic effects in H/R-treated HK-2 cells was abrogated by Akt inhibitor LY294002 supplementation. In summary, the present results demonstrated that HSYA attenuated kidney oxidative stress, inflammation response, and apoptosis induced by I/R, at least in part, via activating the Akt/GSK-3β/Fyn-Nrf2 axis pathway. These findings provided evidence that HSYA may be applied as a potential therapeutic agent in the treatment of I/R induced AKI.

Antioxidant and Anti-Inflammatory Activities of Zingiber montanum Oil in HepG2 Cells and Lipopolysaccharide-Stimulated RAW 264.7 Macrophages.

Improvement of antioxidant and anti-inflammatory functions is believed to be an effective strategy for protection against various diseases such as cancer, aging, and neurodegenerative disease. This study focused on investigating antioxidant and anti-inflammatory abilities of Zingiber montanum oil (ZMO) extracted by the supercritical CO2 fluid system in HepG2 cells and lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Ten predominant constituents of ZMO were identified, in which triquinacene, 1,4-bis (methoxy), terpinen-4-ol, triquinacene, 1,4,7-tris (methoxy), α-terpinene, sabinene hydrate, and (E and Z)-1-(3,4-dimethoxyphenyl)butadiene account for 86.47%. ZMO exhibited anti-inflammatory capacity by inhibiting the formation of pro-inflammatory markers such as nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, interleukin (IL)-1β, IL-6, and monocyte chemoattractant protein-1 in LPS-treated macrophages. The LPS-induced stimulation of nuclear factor-kappa B, signal transducer and activator of transcription 3 (Stat3) and mitogen-activated protein kinase (MAPK) pathways as evident from increased phosphorylation of IKKα/β, IκBα, p65, Stat3, ERK, JNK, and p38 MAPK was also suppressed by ZMO pretreatment. Further, ZMO enhanced the expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1), and concurrently, reduced intracellular reactive oxygen species accumulation in LPS-treated RAW 264.7 cells. In addition, ZMO treatment markedly upregulated the expression of Nrf2 as well as its target genes, HO-1 and NAD(P)H:quinone oxidoreductase 1 in HepG2 cells. These data propose that ZMO may be a potent candidate for prevention and/or treatment of inflammatory and oxidative conditions.

The Effect of Nanocomposite Edible Coating Enriched with Foeniculum vulgare Essential Oil on the Shelf Life of Oncorhynchus mykiss Fish Fillets during the Storage

ABSTRACT In this study, the antioxidant and antimicrobial effect of fennel essential oil in different concentrations of 1%, 1.5%, and 2% (W/V) with three types of nanocoating of basil seed gum, Lepidium perfoliatum, and their combination was examined for extending the life of fish meat. The amount of phenolic compounds for fennel was 80.59 mg g−1. The antioxidant activity of EO was assessed by DPPH and beta-carotene in different concentrations and an increasing trend for antioxidant properties was observed with increasing the EO concentration. Minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) were determined against Staphylococcus aureus, Pseudomonas aeruginosa, and Escherichia coli. The size of the prepared nanocoatings was in the range of 270.80 to 473.21 nm and the zeta potential was negative for all nanocoatings. Fish meat samples were stored at 4°C for 28 days and peroxide value, thiobarbituric acid, S. aureus, E. coli and P. aeruginosa counts, pH, total volatile basic nitrogen (TVN-B), and color changes were measured at 7 day intervals. The use of nanotechnology led to the improvement of antioxidant and antimicrobial properties of coatings. According to the results, the nanocoating of BSG-LPSG containing 2% of fennel EO can be used in meat packaging factories.

ROS MEDIATED MYOCARDIAL ISCHEMIA-REPERFUSION INJURY ATTENUATION BY MORIN: REGULATION OF RISK/SAPK PATHWAYS

Abstract Objective: Morin, a bioflavonoid, has demonstrated anti-oxidant, anti-inflammatory and other diverse pharmacological protective activities in various experimental models. Oxidative stress plays an important role in the pathogenesis of myocardial ischemia reperfusion (IR) injury. Thus, this study aimed to evaluate the effect of Morin in Myocardial IR injury model and its underlying mechanism. Design and method: Male albino Wistar rats were divided into 5 groups. Sham; IR-Control; 2 Morin pre-treated groups (40 and 80 mg/kg; p.o.) and Morin perse group. The morin were administered for 28 days in respective group. On 29th day, rats were experienced 45 min myocardial ischemia following 60 min reperfusion except Sham and Morin perse groups. The cardioprotective potential was investigated via hemodynamic, biochemical, inflammatory marker investigations, cytokines levels, morphological analysis, immuno-histochemical analysis and protein expression estimation through multiplexed Immuno-blotting. The apoptotic markers were also investigate to analysed the programmed cell death due to oxidative stress. Results: With respect to IR-control group, Morin pre-treatment significantly normalized hemodynamic parameters, restored antioxidant status, improved pathological changes, reduced the release of cardiac injury markers, inhibited inflammation (TNF-alpha/IL-6/NF (kappa)B/IKK (beta) and apoptosis (increased Bcl-2, decreased Bax/Caspase-3 and TUNEL positivity) in the myocardium. This improvement in antioxidant, inflammation and anti-apoptosis markers could be due to downregulation of SAPK (p38/JNK) pathway and upregulation of survival kinase i.e. RISK pathway (ERK/eNOS) in the myocardium. Conclusions: IR induced oxidative stress leads to production of free radicals is attenuated by morin pretreatment for 28 days in rats which further reduced inflammation and apoptosis in the myocardium. This is the first experimental study which highlighted the role of SAPK/RISK pathways in morin induced cardio-protection in IR injury.

Gluten free sourdough bread enriched with cricket flour for protein fortification: Antioxidant improvement and Volatilome characterization

Insects represent a novel source of edible high nutritional value proteins which are gaining increasing interest as an alternative to traditional animal foods. In this work, cricket flour was used to produce gluten-free sourdough breads, suitable for celiac people and “source of proteins”. The doughs were fermented by different methods and pH and microbial growth, volatile compounds, protein profile, and antioxidant activity, before and after baking, were analyzed and compared to standard gluten-free doughs. The results showed that cricket-enriched doughs and the standard had similar fermentation processes. Cricket enrichment conferred to the breads a typical flavoring profile, characterized by a unique bouquet of volatile compounds, made by nonanoic acid, 2,4-nonadienal (E,E), 1-hexanol, 1-heptanol, and 3-octen-2-one, expressed in different amounts depending on the type of inoculum. Finally, antioxidant activities were significantly enhanced in cricket breads, indicating that cricket powder provides to bakery gluten-free goods high nutritional value proteins and antioxidant properties.

Attenuation of ROS-mediated myocardial ischemia-reperfusion injury by morin via regulation of RISK/SAPK pathways.

Oxidative stress plays an important role in the pathogenesis of myocardial ischemia-reperfusion (IR) injury. Morin, a bioflavonoid, has demonstrated antioxidant, anti-inflammatory and other diverse pharmacological activities in various experimental models such as isoproterenol-induced myocardial injury, doxorubicin-induced cardiotoxicity and neurotoxicity, as well as cisplatin-induced nephrotoxicity. Thus, this study aimed to evaluate the effect of morin in myocardial IR injury model and its underlying mechanisms. To accomplish this, male albino Wistar rats were pre-treated with morin (40 and 80mg/kg; po) for 28days and on 29th day, rats experienced 45-min myocardial ischemia followed by 60-min reperfusion. In comparison to IR-control group, morin pre-treatment significantly normalized hemodynamic parameters, restored antioxidant status, improved pathological changes, reduced the release of cardiac injury markers, inhibited inflammation (TNF-α/IL-6/NFκB/IKKβ) and apoptosis (increased Bcl-2, decreased Bax/Caspase-3 and TUNEL positivity) in the myocardium. This improvement in antioxidant, inflammation and anti-apoptosis markers could be due to downregulation of SAPK (p38/JNK) pathway and upregulation of survival kinase, i.e. RISK pathway (ERK/eNOS) in the myocardium. Thus, morin attenuated myocardial IR injury in rats by regulation of RISK/SAPK pathways.

Improvement of antioxidant and antimicrobial activity of soy isoflavones extracts bioconverted with β-glucosidase

Improvement of antioxidant and antimicrobial activity of soy isoflavones extracts bioconverted with β-glucosidase

Plasma Oxidative Status in Preterm Infants Receiving LCPUFA Supplementation: A Pilot Study

After birth, preterm infants are deficient in arachidonic acid (ARA), docosahexaenoic acid (DHA), and antioxidants, increasing their risk of oxidative stress-related pathologies. The principal aim was to evaluate if supplementation with long-chain polyunsaturated fatty acids (LCPUFAs) improves antioxidant defenses. In total, 21 preterm infants were supplemented with ARA and DHA in a 2:1 ratio (ARA:DHA-S) or with medium-chain triglycerides (MCT-S). Plasma n-3 and n-6 LCPUFAs were measured at birth, postnatal day 28, and 36 weeks of postmenstrual age (36 WPA) by gas chromatography–mass spectroscopy. Plasma antioxidants (glutathione (GSH), catalase, and thiols) and oxidative damage biomarkers (malondialdehyde (MDA), carbonyls) were analyzed at the same time points by spectrophotometry, and scores of antioxidant status (Antiox-S) and oxidative damage (Proxy-S) were calculated. At 36 WPA, linoleic acid (LA) and dihomo-γ-linolenic acid (DGLA) were decreased in ARA:DHA-S compared to the MCT-S group (LA: ARA:DHA-S = 18.54 ± 1.68, MCT-S = 22.80 ± 1.41; p = 0.018; DGLA: ARA:DHA-S = 1.68 ± 0.38, MCT-S = 2.32 ± 0.58; p = 0.018). Furthermore, α-linolenic acid (ALA) was increased in ARA:DHA-S (ARA:DHA-S = 0.52 ± 0.33, MCT-S = 0.22 ± 0.10; p = 0.018). Additionally, LA:DHA ratio was decreased in the ARA:DHA-S compared to control group (ARA:DHA-S = 6.26 ± 2.35, MCT-S = 8.21 ± 2.65; p = 0.045). By the end of supplementation (36 WPA), catalase, thiol groups, and Antiox-S were significantly higher in neonates receiving ARA:DHA-S compared to those receiving MCT-S, with no differences in oxidative stress biomarkers. In conclusion, ARA:DHA supplementation in preterm neonates resulted in an overall improvement in antioxidant to oxidant balance and a decrease in early fatty acid precursors of the n-6 relative to the n-3 pathway. These effects may reduce oxidative stress and inflammation.

Preparation of Silver Sulfadiazine Loaded Pectin-Zinc Nanocomposites for Improvement of Antioxidant, Antibacterial and Care Cutaneous Wound Care During the Perioperative Period

Medicinal care for cutaneous wound becomes difficult due to the emergence of antibiotic resistant bacteria. The development of a new cost-effective drug based on silver sulfadiazine loaded with pectin-zinc nanocomposites offers better therapeutics in wound healing besides its role in enhancing antioxidant and antibacterial activities. In this study, silver sulfadiazine loaded with pectin-zinc nanocomposites (AgSD-PC-Zn) was produced and its antioxidant and antimicrobial properties were tested against wound infection causing bacterial pathogens (S. aureus and E. coli). The synthesized AgSD-PC-Zn composite was biophysically characterized. TEM analysis confirmed the spherical shape of NPs. AgSD-PC-Zn composite exhibited a greater antibacterial effect against S. aureus and E. coli. The number of dead bacterial cells was higher after exposure to AgSD-PC-Zn composite. Furthermore, in vitro antioxidant enzyme activities (DPPH and H2O2) were increased with AgSDPC-Zn composite. A rapid healing of the skin wounds in mouse was noticed with AgSD-PC-Zn composite treatment. This study concludes that the newly formed AgSD-PC-Zn composite will act as a strong antimicrobial and antioxidant agents for treating skin wound infection.

Effective hydroxylation of tangeretin from Citrus Peel (Chenpi) by edible acids and its improvement in antioxidant and anti-lipase activities

Tangeretin (TAN) is a biologically functional polymethoxylated flavonoid, extracted from the Citrus Peel (Chenpi). Although 5-demethyltangeretin (5-DT) generated through hydrolysis using a TAN precursor has superior biological function to TAN, its traditional preparation methods are difficult due to environmental hazard and low efficiency processes. In this study, the phosphoric acid (a kind of edible acids) was screened as catalysts of TAN hydrolysis conversion to 5-DT. The main conversion-influencing factors of reaction (material/liquid ratio, temperature and time) were investigated and the antioxidant activity of the modified products was determined by measuring DPPH (Diphenylpicrylbenzoquinone) free radical scavenging capacity and total reducing power. The phosphoric acid/ethanol (v/v) ratio of 7:3, material/liquid (g/L) ratio of 2:1, conversion temperature of 175 °C and conversion time of 2 h were attained as optimal conditions with a 93.71% conversion rate. Further, in vitro antioxidant and anti-lipase experiments confirmed that 5-DT was superior to TAN in total reducing power, scavenging capacity of DPPH free radicals (p < 0.01) and inhibition of lipase activities. Therefore, phosphoric acid is proposed as an alternative catalyst for the modification of TAN. Further, it provided technical support for the industrial production of 5DT and its application in functional foods.

Effects of Endurance Exercise Training on Cardiac Dysfunction Induced by Waterpipe Tobacco Smoking.

BackgroundThere is an increasing popularity of waterpipe tobacco smoking (WTS) in youth and even in athletes worldwide. Despite the existence of evidence of the harmful effects of hookah smoke on various systems of the body, especially the cardiovascular system, its simultaneous effect with exercise training has not been well studied. We assessed the effects of WTS exposure with/without swimming exercise on blood pressure (BP), and heart histology and mechanical performance in male Wistar rats.MethodsThe animals were divided into 4 groups of sedentary control (CTL), waterpipe tobacco smoking (S), mild endurance swimming exercise training (Ex), and waterpipe smoking plus exercise (S + Ex). The duration of WTS and exercise was 8 weeks.FindingsBP and heart rate (HR) did not show a significant difference among the groups. WTS increased the TNF-α level of the heart (P < 0.05 vs. CTL) and cardiac tissue lesions (P < 0.05 vs. CTL), and reduced +dP/dt max, -dp/dt max, and heart contractility indices (P < 0.01, P < 0.01, and P < 0.05, respectively, vs. CTL and Ex groups). It also increased the Tau index (P < 0.05 vs. CTL; P < 0.01 vs. Ex groups) of the left ventricle. However, the combination of exercise and WTS reduced the TNF-α level, improved the heart activity of superoxide dismutase (SOD) and catalase enzymes, and prevented the negative effects of smoking on heart function and morphology.ConclusionMild exercise prevents WTS-induced left ventricular systolic and diastolic dysfunction partly via improvement of antioxidants and attenuation of pro-inflammatory cytokines.

TRAF1 meditates lipopolysaccharide-induced acute lung injury by up regulating JNK activation

Acute lung injury (ALI) is served as a severe life-threatening disease. However, the pathogenesis that contributes to ALI has not been fully understood. Tumor necrosis factor receptor-associated factor 1 (TRAF1) interacts with multiple regulators, performing its diverse role in biological functions. However, the effects of TRAF1 on ALI remain unknown. In this study, we attempted to explore the role of TRAF1 in ALI progression. The findings suggested that TRAF1-knockout (KO) markedly attenuated LPS-induced severe mortality rate in murine animals. LPS-elicited histological alterations in pulmonary tissues were significantly alleviated by TRAF1-deletion. Additionally, TRAF1 knockout effectively attenuated lung injury, as evidenced by the reduced lung wet/dry (W/D) weight ratio, as well as decreased bronchoalveolar lavage fluid (BALF) protein levels and neutrophil infiltration. Meanwhile, TRAF1 deletion markedly lessened inflammation, oxidative stress and apoptosis in BALF and/or lung tissues. The levels of pro-inflammatory cytokines stimulated by LPS were down-regulated by TRAF1 ablation, along with the inactivation of nuclear factor κB (NF-κB). LPS-promoted reactive oxygen species (ROS) generation was decreased in TRAF1-KO mice, partly through the improvement of anti-oxidants. Apoptosis was also inhibited by TRAF1 deletion in lung tissues of LPS-challenged mice through the suppression of cleaved Caspase-3. Moreover, TRAF1 knockout significantly decreased c-Jun N-terminal kinase (JNK) activation and its down-streaming signal of c-Jun in pulmonary samples of LPS-induced mice. Importantly, the in vitro study suggested that promoting JNK activation markedly abrogated TRAF1 knockdown-attenuated inflammation, ROS production and apoptosis in LPS-exposed A549 cells. Therefore, our experimental results provided evidence that TRAF1 suppression effectively protected LPS-induced ALI against inflammation, oxidative stress and apoptosis through the suppression of JNK activity.

Pré‐condicionamento com dexmedetomidina protege contra lesão pulmonar em ratos com choque hemorrágico

Background and objectivesDexmedetomidine has demonstrated protective effects against lung injury in vitro. Here, we investigated whether dexmedetomidine preconditioning protected against lung injury in hemorrhagic shock rats. MethodsMale Sprague‐Dawley rats were randomly divided into four groups (n=8): control group, hemorrhagic shock group, 5ug.kg−1 dexmedetomidine (DEX1) group, and 10ug.kg−1 dexmedetomidine (DEX2) group. Saline or dexmedetomidine were administered over 20min. 30min after injection, hemorrhage was initiated in the hemorrhagic shock, DEX1 and DEX2 group. Four hours after resuscitation, protein and cellular content in bronchoalveolar lavage fluid, and the lung histopathology were measured. The malondialdehyde, superoxide dismutase, Bcl‐2, Bax and caspase‐3 were also tested in the lung tissue. ResultsCompare with hemorrhagic shock group, 5ug.kg−1 dexmedetomidine pretreatment reduced the apoptosis (2.25±0.24 vs. 4.12±0.42%, p<0.05), histological score (1.06±0.12 vs. 1.68±0.15, p<0.05) and protein (1.92±0.38 vs. 3.95±0.42mg.mL−1, p<0.05) and WBC (0.42±0.11 vs. 0.92±0.13×109/L, p<0.05) in bronchoalveolar lavage fluid. Which is correlated with increased superoxide dismutase activity (8.35±0.68 vs. 4.73±0.44U.mg−1 protein, p<0.05) and decreased malondialdehyde (2.18±0.19 vs. 3.28±0.27nmoL.mg−1 protein, p<0.05). Dexmedetomidine preconditioning also increased the Bcl‐2 level (0.55±0.04 vs. 0.34±0.05, p<0.05) and decreased the level of Bax (0.46±0.03 vs. 0.68±0.04, p<0.05), caspase‐3 (0.49±0.03 vs. 0.69±0.04, p<0.05). However, we did not observe any difference between the DEX1 and DEX2 groups for these (p>0.05). ConclusionDexmedetomidine preconditioning has a protective effect against lung injury caused by hemorrhagic shock in rats. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation. But did not show a dose‐dependent effect.

Dexmedetomidine preconditioning protects against lung injury in hemorrhagic shock rats

Background and objectivesDexmedetomidine has demonstrated protective effects against lung injury in vitro. Here, we investigated whether dexmedetomidine preconditioning protected against lung injury in hemorrhagic shock rats. MethodsMale Sprague-Dawley rats were randomly divided into four groups (n=8): control group, hemorrhagic shock group, 5ug.kg−1 dexmedetomidine (DEX1) group, and 10ug.kg−1 dexmedetomidine (DEX2) group. Saline or dexmedetomidine were administered over 20min. 30min after injection, hemorrhage was initiated in the hemorrhagic shock, DEX1 and DEX2 group. Four hours after resuscitation, protein and cellular content in bronchoalveolar lavage fluid, and the lung histopathology were measured. The malondialdehyde, superoxide dismutase, Bcl-2, Bax and caspase-3 were also tested in the lung tissue. ResultsCompare with hemorrhagic shock group, 5ug.kg−1 dexmedetomidine pretreatment reduced the apoptosis (2.25±0.24 vs. 4.12±0.42%, p<0.05), histological score (1.06±0.12 vs. 1.68±0.15, p<0.05) and protein (1.92±0.38 vs. 3.95±0.42mg.mL−1, p<0.05) and WBC (0.42±0.11 vs. 0.92±0.13×109/L, p<0.05) in bronchoalveolar lavage fluid. Which is correlated with increased superoxide dismutase activity (8.35±0.68 vs. 4.73±0.44U.mg−1 protein, p<0.05) and decreased malondialdehyde (2.18±0.19 vs. 3.28±0.27nmoL.mg−1 protein, p<0.05). Dexmedetomidine preconditioning also increased the Bcl-2 level (0.55±0.04 vs. 0.34±0.05, p<0.05) and decreased the level of Bax (0.46±0.03 vs. 0.68±0.04, p<0.05), caspase-3 (0.49±0.03 vs. 0.69±0.04, p<0.05). However, we did not observe any difference between the DEX1 and DEX2 groups for these (p>0.05). ConclusionDexmedetomidine preconditioning has a protective effect against lung injury caused by hemorrhagic shock in rats. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation. But did not show a dose-dependent effect.

Protective effects of silymarin on triptolide-induced acute hepatotoxicity in rats.

Silymarin has been used in the treatment of a number of liver diseases for a long time, but its efficacy in preventing triptolide induced acute hepatotoxicity has not been reported previously. The present study aimed to assess the protective effect of silymarin against triptolide (TP)-induced hepatotoxicity in rats. Rats were orally administrated with silymarin (50, 100 and 200 mg/kg) for 7 days and received intraperitoneal TP (2 mg/kg) on the day 8. Hepatic injuries were comprehensively evaluated in terms of serum parameters, morphological changes, oxidative damage, inflammation and apoptosis. The results demonstrated that TP-induced increases in serum parameters, including alanine transaminase, aspartate aminotransferase, alkaline phosphatase, total cholesterol and γ-glutamyl transpeptidase, which were determined using a biochemical analyzer, and histopathological alterations and hepatocyte apoptosis as determined by hematoxylin and eosin and TUNEL staining, respectively, were prevented by silymarin pretreatment in a dose-dependent manner. TP-induced depletions in the activity of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, glutathione S-transferase and catalase, and glutathione levels, were also significantly reversed by silymarin, as determined using specific kits. Additionally, silymarin dose-dependently exhibited inhibitory effects on malonaldehyde content in the liver. The production of proinflammatory cytokines was investigated using ELISA kits, and the results demonstrated that silymarin dose-dependently inhibited the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10 and IL-1β in the liver. To determine the mechanism of silymarin, western blot analysis was performed to investigate the protein expression of phosphorylated (p)-p38 and p-c-Jun N-terminal kinase (JNK) of the TNF-α induced inflammatory response and apoptotic pathways. Silymarin significantly blocked p38 and JNK phosphorylation and activation. Additionally, the expression of the proapoptotic proteins cytochrome c, cleaved caspase-3 and Bcl-2-associated X was also reduced following treatment with silymarin, as determined by ELISA, western blotting and immunohistochemistry, respectively. In conclusion, silymarin was demonstrated to dose-dependently protect rat liver from TP-induced acute hepatotoxicity, with the high dose (200 mg/kg) achieving a superior effect. This protective effect may be associated with the improvement of antioxidant and anti-inflammatory status, as well as the prevention of hepatocyte apoptosis. Therefore, silymarin may have the potential to be applied clinically to prevent TP-induced acute hepatotoxicity.