Cromolyn Sodium Attenuates Paraquat-Induced Lung Injury by Modulation of Proinflammatory Cytokines

Larki‐Harchegani, Amir; Hemmati, Ali Asghar; Nili‐Ahmadabadi, Amir; Darabi, Borhan; Shabib, Somayeh

doi:10.1055/s-0042-123711

Cited by 35 publications

(14 citation statements)

References 27 publications

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“…Consistent with our previous findings [43], paraquat acted as a systemic stressor, as evidenced by its elevation of plasma corticosterone and IL-6, provocation of sickness behavior, and disturbances in nesting and motor behaviors. Indeed, we and others have shown that paraquat-induced increased pro-inflammatory cytokine levels in the brain, as well as in the lungs and in serum [19, 32, 44–46]. We know that collectively these cytokines and corticosterone can act additively or even synergistically to provoke behavioral disturbances and neurochemical alterations and at high enough concentration can cause cellular death [47, 48].…”

Section: Discussionmentioning

confidence: 99%

Leucine-rich repeat kinase-2 (LRRK2) modulates paraquat-induced inflammatory sickness and stress phenotype

Rudyk

Dwyer

Hayley

2019

J Neuroinflammation

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Background Leucine-rich repeat kinase 2 (LRRK2) is a common gene implicated in Parkinson’s disease (PD) and is also thought to be fundamentally involved in numerous immune functions. Thus, we assessed the role of LRRK2 in the context of the effects of the environmental toxicant, paraquat, that has been implicated in PD and is known to affect inflammatory processes. Methods Male LRRK2 knockout (KO) and transgenic mice bearing the G2019S LRRK2 mutation (aged 6–8 months) or their littermate controls were exposed to paraquat (two times per week for 3 weeks), and sickness measures, motivational scores, and total home-cage activity levels were assessed. Following sacrifice, western blot and ELISA assays were performed to see whether or not LRRK2 expression would alter processes related to plasticity, immune response processes, or the stress response. Results Paraquat-induced signs of sickness, inflammation (elevated IL-6), and peripheral toxicity (e.g., organ weight) were completely prevented by LRRK2 knockout. In fact, LRRK2 knockout dramatically reduced not only signs of illness, but also the motivational (nest building) and home-cage activity deficits induced by paraquat. Although LRRK2 deficiency did not affect the striatal BDNF reduction that was provoked by paraquat, it did blunt the corticosterone elevation induced by paraquat, raising the possibility that LRRK2 may modulate aspects of the HPA stress axis. Accordingly, we found that transgenic mice bearing the G2019S LRRK2 mutation had elevated basal corticosterone, along with diminished hippocampal 5-HT1A levels. Conclusion We are the first to show the importance of LRRK2 in the peripheral neurotoxic and stressor-like effects of paraquat. These data are consistent with LRRK2 playing a role in the general inflammatory tone and stressor effects induced by environmental toxicant exposure.

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Section: Discussionmentioning

confidence: 99%

Leucine-rich repeat kinase-2 (LRRK2) modulates paraquat-induced inflammatory sickness and stress phenotype

Rudyk

Dwyer

Hayley

2019

J Neuroinflammation

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“…The injection volume was 0.2 mL for each animal. At the end of study course, the mice were weighed and then anaesthetized with ketamine at 50 mg/kg and xylazine 10 mg/kg(13).…”

Section: Methodsmentioning

confidence: 99%

Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study

et al. 2018

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Thymoquinone (TQ) is the main active constituent of Nigella sativa seeds. The objective of this study was to explore the protective effects of TQ on diazinon (DZN)-induced liver toxicity in the mouse model. The animals were divided into five groups of 6 each and treated intraperitoneally. Group 1 received the vehicle, group 2 was given 16 mg/kg DZN, group 3 received 5 mg/kg TQ, and groups 4 and 5 were treated with 1.25 and 5 mg/kg of TQ as well as 16 mg/kg DZN, respectively. Finally, butyrylcholinesterase (BChE), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) serum activity as well as nitric oxide (NO), lipid peroxidation (LPO), total antioxidant capacity (TAC), total thiol molecule (TTM), and histopathological experiments were evaluated in the liver samples. Our findings showed that DZN caused a significant increase in ALT (P < 0.01), AST (P < 0.001), ALP (P < 0.001) serum levels, LPO (P < 0.001) and NO (P < 0.001), the depletion of the TAC (P < 0.05) and TTM (P < 0.001), and structural changes in the liver tissue. Following TQ administration, a significant improvement was observed in the oxidative stress biomarkers in the liver tissue. In addition, our biochemical findings were correlated well to the histopathological examinations. In conclusion, the data from this study indicate that the administration of TQ may prevent liver damage by preventing free radical formation in animals exposed to DZN.

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“…istopathological assessment was used at 200 x (scale bar = 100 μm) and 400 x (scale bar = 20 μm) magnification (Olympus BX51, Tokyo, Japan). Any changes in morphology such as infiltration of inflammatory cells, congestion, hemorrhage or hyperemia, necrosis were evaluated [21].…”

Section: Histopathological Reportmentioning

confidence: 99%

Short-term Effects of Metformin on Cardiac and Peripheral Blood Cells Following Cecal Ligation and Puncture-induced Sepsis

et al. 2020

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Aim of the study Sepsis has well-documented inflammatory effects on cardiovascular and blood cells. This study is designed to investigate potential anti-inflammatory effects of metformin on cardiac and blood cells 12 and 24 h following cecal ligation and puncture (CLP)-induced sepsis. Methods For the purpose of this study, 36 male Wistar rats were divided into six groups: two groups underwent CLP, two groups underwent CLP and received metformin, and two groups only received sham operations. 12 h later, 18 rats (half of rats in each of the three aforementioned groups) were sacrificed and cardiac and blood cells were harvested. Subsequently, 12 h later, the rest of the rats were euthanatized. In all harvested blood and cardiac cells, oxidative stress indicators, antioxidant properties, count of blood cells, neutrophil infiltration, percentage of weight loss and pathological assessment were conducted. Results In our experiment, metformin elevated antioxidant levels, improved function of blood cells and percentage of weight loss. Moreover, in the groups which received metformin, oxidative stress and neutrophil infiltration markers were decreased significantly. Moreover, pathological investigations of cardiac cell injury were reduced in the metformin group. Conclusions Our findings suggest that in CLP induced sepsis model, metformin can improve the function of blood and cardiac cells through alleviating inflammation, improvement of anti-inflammation properties, and enhancement of blood profile, and all these effects are more pronounced after 24 h in comparison with 12 h after induction of sepsis.

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Cromolyn Sodium Attenuates Paraquat-Induced Lung Injury by Modulation of Proinflammatory Cytokines

Cited by 35 publications

References 27 publications

Leucine-rich repeat kinase-2 (LRRK2) modulates paraquat-induced inflammatory sickness and stress phenotype

Leucine-rich repeat kinase-2 (LRRK2) modulates paraquat-induced inflammatory sickness and stress phenotype

Thymoquinone attenuates hepatotoxicity and oxidative damage caused by diazinon: an in vivo study

Short-term Effects of Metformin on Cardiac and Peripheral Blood Cells Following Cecal Ligation and Puncture-induced Sepsis

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