Protective effect of sodium aescinate on lung injury induced by methyl parathion

Du, Yuan; Wang, Tian; Jiang, Na; Ren, Rutong; Zhao, Deyu; Li, Chong; Fu, Fenghua

doi:10.1177/0960327110393764

Cited by 14 publications

(8 citation statements)

References 34 publications

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“…Thus, the effects of SA on myocardial apoptosis induced by MP have also been investigated.. Sodium aescinate could also protect against lung injury induced by intestinal ischemia/reperfusion (I/R) by regulating the expression of Bcl-2 and Bax proteins and inhibiting the apoptosis of lung cells [9]. This research demonstrate that SA can exert cardio-protective effect by inhibiting MP-induced apoptosis of myocardial cells.…”

Section: Discussionmentioning

confidence: 84%

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Effect of sodium aescinate on methyl parathion-induced myocardial injury in rats

Wen¹,

Su²,

Luo³

et al. 2019

Trop. J. Pharm Res

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Purpose: To explore the effects and mechanism of sodium aescinate (SA) on methyl parathion (MP)induced myocardial injury. Methods: Rats were divided into following groups: In Control group, rats were administered 0.9 % NaCl by intraperitoneal injection. In MP group, rats were administered 20 mg/kg MP by intraperitoneal injection. In MP + SA group, rats were administered 20 mg/kg MP in combination with SA at a concentration of 0.5, 1.0, or 1.5 mg/kg by intraperitoneal injection. Histological changes were assessed by H&E staining. Serum levels of cardiac troponin T (CTnT) and atrial natriuretie peptide (ANP) were measured by automatic biochemical analyzer and real-time polymerase chain reaction (RT-PCR), respectively. The levels of malondiadehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) in heart tissue was detected by spectrophotometry. The apoptosis of myocardial cells was measured by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. The level of apoptosis-related proteins was assessed by western blot. Results: Superoxide dismutase attenuated MP-induced myocardial injury, and decreased the levels of ANP and cTnT in serum (p < 0.01). Superoxide dismutase attenuated the MP-induced decrease in GSH, GSH-px, and SOD expression (p < 0.05) but increased MDA level (p < 0.01). Moreover, SA inhibited the apoptosis of myocardial cells and regulation of apoptosis-related protein expression (e.g., Bax, Bcl-2, and caspase 3). Conclusion: These results demonstrate that SA attenuates MP-induced myocardial injury by regulating oxidative stress and apoptosis.

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Section: Discussionmentioning

confidence: 84%

“…Thus, the effects of SA in clinics include antiinflammation, anti-oxidation, and regulation of microcirculation [8]. Researchers found that SA can attenuate MP-induced lung injury via antiinflammatory and anti-oxidative effects [9]. However, the effects of SA on MP-induced myocardial injury remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Effect of sodium aescinate on methyl parathion-induced myocardial injury in rats

Wen¹,

Su²,

Luo³

et al. 2019

Trop. J. Pharm Res

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“…SA has potent anti-inflammatory, anti-edematous and anti-oxidative activity by enhancing glucocorticoid and its receptor expression (Du et al, 2011; Montopoli et al, 2007; Wang et al, 2009; Wang et al, 2012; Wei et al, 2011; Xin et al, 2011; Yang et al, 2011). Accordingly, the effect of SA treatment on the PGPS-induced inflammation was investigated in Tlr2 −/− mice.…”

Section: Resultsmentioning

confidence: 99%

Otitis media induced by peptidoglycan-polysaccharide (PGPS) in TLR2-deficient (Tlr2−/−) mice for developing drug therapy

Zhang

Zheng

Sang

et al. 2015

Infection, Genetics and Evolution

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Background Toll like receptor 2 (TLR2) signaling can regulate the pathogenesis of otitis media (OM). However, the precise role of TLR2 signaling in OM has not been clarified due to the lack of an optimal animal model. Peptidoglycan-polysaccharide (PGPS) of the bacterial cell wall can induce inflammation by activating the TLR2 signaling. This study aimed at examining the pathogenic characteristics of OM induced by PGPS in Tlr2−/− mice, and the potential therapeutic effect of Sodium aescinate (SA) in this model. Methods Wild-type (WT) and Tlr2−/− mice were inoculated with streptococcal PGPS into their middle ears (MEs) and treated intravenously with vehicle or SA daily beginning at 3 days prior to PGPS for 6 consecutive days. The pathologic changes of individual mice were evaluated longitudinally. Results In comparison with WT mice, Tlr2−/− mice were susceptible to PGPS-induced OM. Tlr2−/− mice displayed greater hearing loss, tympanic membrane damage, ME mucosal thickening, longer inflammation state, cilia and goblet cell loss. SA-treatment decreased neutrophil infiltration, modulated TLR2-related gene expression and improved ciliary organization. Conclusions PGPS induced a relatively stable OM in Tlr2−/− mice, providing a new model for OM research. Treatment with SA mitigated the pathogenic damage in the ME and may be valuable for intervention of OM.

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“…4 It is also reported that the organophosphorus-treated rats showed lung injury characterized by oxidative stress and inflammation. 5 Panax ginseng Meyer is a well-known medicinal plant from eastern Asian countries, especially China, Korea, and Japan. Ginsenosides are the bioactive ingredients of ginseng that is used widely in traditional medicine.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg3 attenuated omethoate-induced lung injury in rats

Wang

Zhao

et al. 2015

Hum Exp Toxicol

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Organophosphorus exposure affects different organs such as the lung, gastrointestinal tract, liver, and brain. The present experiment aimed to evaluate the effect of ginsenoside Rg3 on lung injury induced by acute omethoate poisoning. Rats were administered with omethoate subcutaneously at a single dose of 60 mg/kg, followed by ginsenoside Rg3 (5, 10, or 20 mg/kg) treatment. Histopathological examination of the lung was performed at 24 h after the omethoate exposure. The antioxidative parameters in the lung were also assayed. Moreover, the activities of acetylcholinesterase, myeloperoxidase, and the content of tumor necrosis factor α (TNF-α) in the lung were determined. The results showed that ginsenoside Rg3 attenuated omethoate-induced lung injury. Ginsenoside Rg3 increased the level of glutathione in the lung ( p < 0.05 or p < 0.01). The altered activities of superoxide dismutase and catalase in the lung were also ameliorated by ginsenoside Rg3 treatment ( p < 0.05 or p < 0.01). Ginsenoside Rg3 caused significant reductions in the contents of malondialdehyde, TNF-α, and the activity of myeloperoxidase ( p < 0.05 or p < 0.01). The present study demonstrated that ginsenoside Rg3 had a protective effect against omethoate-induced lung injury in rats, and the mechanisms were related to its antioxidant potential and anti-inflammatory effect.

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Protective effect of sodium aescinate on lung injury induced by methyl parathion

Cited by 14 publications

References 34 publications

Effect of sodium aescinate on methyl parathion-induced myocardial injury in rats

Effect of sodium aescinate on methyl parathion-induced myocardial injury in rats

Otitis media induced by peptidoglycan-polysaccharide (PGPS) in TLR2-deficient (Tlr2−/−) mice for developing drug therapy

Ginsenoside Rg3 attenuated omethoate-induced lung injury in rats

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