Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Meng, Xiaoxiao; Wang, Ruilan; Gao, Shan; Xie, Hui; Tan, Jing‐Yu; Qian, Yongbing

doi:10.5847/wjem.j.issn.1920-8642.2013.02.009

Cited by 14 publications

(8 citation statements)

References 21 publications

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“…Exposure to environmental hazards including herbicides is one of the challenges that faces the scientists to discover and measure the safety of human health especially in occupational exposure that affect the people medical social and economic sides. Oxidative stress and radicals has been recorded to be the major mechanism causing paraquat (PQ) toxicity [41].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Hesperidin and Benfotiamine against Paraquat Induced Spinal Cord Neurotoxicity in Adult Male Albino Rats

Amin¹,

Ameen²,

Abaza³

2021

ODEM

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Introduction: There are extensive people exposures to paraquat (PQ) herbicide resulting in human health hazards. Aim of the Work: To compare the beneficial neuroprotective effects of hesperidin and benfotiamine on paraquat (PQ)-induced spinal cord neurotoxic effects in rats. Materials and Methods: Rats were divided into 4 groups as following: control, paraquat (PQ 20.8 mg/kg, oral gavage (e.g.)), paraquat + benfotiamine (50 mg/kg, oral gavage (e.g.)) and paraquat + hesperidin (40 mg/kg, oral gavage (e.g.)). PQ is given as the previous dose. Rats are treated 6 days per week. Results: There was a significant increased mean value of malondialdehyde associated with a significant reduction in the content of reduced glutathione and antioxidant enzymes activities associated with a significant increase in Serum phosphorylated neurofilament-H, neurospecific enolase and s100 levels were recorded and significant spinal cord histopathological changes in paraquat treated group as compared to their corresponding values in the control group and immunohistochemical examination confirmed these results. Upon supplementation with benfotiamine and hesperidin to paraquat treated rats, there was a significant decrease in the mean values of malondialdehyde associated with a marked increase in the content of reduced glutathione and antioxidant enzymes activities associated with a significant decrease in Serum phosphorylated neurofilament-H, neurospecific enolase and s100 levels were also recorded with significant improvement of spinal cord architecture when compared with the paraquat treated group. Conclusion: The use of benfotiamine and hesperidin produced a significant protection against all of the above-mentioned changes.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Hesperidin and Benfotiamine against Paraquat Induced Spinal Cord Neurotoxicity in Adult Male Albino Rats

Amin¹,

Ameen²,

Abaza³

2021

ODEM

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“…The determination of SOD and MDA could refl ect the ability of scavenging oxygen free radicals and the anti-lipid peroxidation damage, respectively. [7] Studies [5,6] have reported that PQ might exert its cytotoxicity through mitochondrial dysfunction. Mitochondrial dysfunction is one of the manifestations that free radicals attack the body.…”

Section: Discussionmentioning

confidence: 99%

Effect of SP-A/B in lipoic acid on acute paraquat poisoning

Han

Sun

et al. 2014

World Journal of Emergency Medicine

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BACKGROUND: This study was undertaken to observe the concentration of SP-A/B and the pulmonary surfactant in the lung tissue of rats with acute lung injury/acute respiratory distress syndrome caused by paraquat poisoning after the treatment of metabolic antioxidant-lipoic acid and whether its infl uence was related to TNF-α. METHODS:Sixty-six male Sprage-Dawley rats were randomly divided into three groups: normal control group (NS group), 6 rats; paraquat poisoning group (PQ group), 30 rats; and paraquat+lipoic acid treatment group (LA group), 30 rats. The rats in the PQ and LA groups were subdivided into 3-, 6-, 12-, 24-, 48-hour subgroups, with 6 rats in each group. After the rats were sacrifi ced, lung tissue from the same part was taken from the rats. After HE staining, histological changes were observed in the tissue under a light microscope. Lung tissue was also taken to test the levels of superoxide dismutase (SOD) and malondialdehyde (MDA). Whole blood (0.8 mL) without anticoagulant was drawn from the tail vein of rats for the determination of the TNF-α level. The total RNA of the lung tissue was collected, and the Rt-PCR method was used to measure the levels of SP-A and SP-B mRNA.RESULTS: HE staining showed that histopathological changes were milder in the LA group than in the PQ group. There were signifi cant differences in MDA and SOD levels between different intervals both in intergroups and intragroups except the 3-hour subgroup (P<0.01). Likewise, the significant differences in the levels of TNF-α were also present between the three groups and between different intervals (P<0.01). The significant differences in SP-A mRNA and SP-B mRNA amplification ratio were seen between the three groups at the same intervals (P<0.01), but the differences between different intervals in the PQ group were statistically significant (P<0.05). The differences between different intervals in the LA group were statistically signifi cant (P<0.01).CONCLUSION: Lipoic acid in acute paraquat poisoning could diminish lung tissue damage by regulating directly tumor necrosis factor and indirectly the content of pulmonary surfactant so as to reduce pulmonary edema, improve lung compliance, and fi nally protect lung tissues.

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“…According to the latest research survey, 80% of white-collar workers in China are in the state of overfatigue at present. About 95.7% of young people have died of fatigue-related fatal diseases [1]. According to statistics, the annual incidence of sudden death in Western European and American countries is 0.1-0.2%.…”

Section: Epidemiologymentioning

confidence: 99%

“…Haiyan Zhu 1,2 *, Guoxin Han 3 and Shuoshuo Li 1 1 Emergency Department, The First Medical Center of Chinese PLA General Hospital, Beijing, China…”

Section: Author Detailsmentioning

confidence: 99%

Chronic Fatigue Stress and Sudden Death

Zhu

Han

Li³

2020

Effects of Stress on Human Health

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Stress refers to a series of neuroendocrine reactions, such as sympathetic nerve excitation and pituitary-adrenal cortex secretion increase, which occur when the body is stimulated by various stressors, and the changes of various functions and metabolism caused by these reactions. Chronic fatigue stress is a fatigue state caused by long-term physical and psychological stress. When the stress reaches a certain intensity or the individual is not well-tolerated, the body stability is impaired, resulting in various pathophysiological reactions leading to various diseases, such as stress hyperglycemia, stress cardiomyopathy, stress arrhythmia, stress ulcer hemorrhagic shock, or even stress ulcer hemorrhagic shock. Eventually lead to sudden death and other adverse events.

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Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Cited by 14 publications

References 21 publications

Neuroprotective Effects of Hesperidin and Benfotiamine against Paraquat Induced Spinal Cord Neurotoxicity in Adult Male Albino Rats

Neuroprotective Effects of Hesperidin and Benfotiamine against Paraquat Induced Spinal Cord Neurotoxicity in Adult Male Albino Rats

Effect of SP-A/B in lipoic acid on acute paraquat poisoning

Chronic Fatigue Stress and Sudden Death

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