Protective Effects of Asiatic Acid Against Spinal Cord Injury-Induced Acute Lung Injury in Rats

Jiang, Wu; Li, Maoqiang; He, Fangping; Yao, Wangxiang; Bian, Zhenyu; Wang, Xuepeng; Zhu, Liangliang

doi:10.1007/s10753-016-0414-3

Cited by 30 publications

(25 citation statements)

References 42 publications

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“…LPS triggers similar pathological processes to those observed in ALI . Neutrophil accumulation results in the production of reactive oxygen species and granular enzymes, leading to lung tissue damage via induction of an inﬂammatory cascade . In this study, we observed a significant increase in MPO activity in lung tissue after LPS injury.…”

Section: Discussionsupporting

confidence: 80%

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

Lin

Hou

et al. 2019

J Biochem & Molecular Tox

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We investigated the effects and associated mechanism of alkannin (AL) on lipopolysaccharide (LPS)-induced acute lung injury in a mouse model. Pretreatment with AL in vivo significantly reduced the lung wet/dry weight ratio and inhibited lung myeloperoxidase activity and malondialdehyde content, while increasing superoxide dismutase activity. Hematoxylin and eosin staining demonstrated that AL attenuated lung histopathological changes. In addition, AL-inhibited overproduction of proinflammatory cytokines in bronchoalveolar lavage fluid and lung tissues in LPS-injured mice and LPS-exposed A549 cells. Further analysis showed that AL-inhibited induction of the Rho/ROCK/NF-κB pathway via LPS-induced inflammation in mice and A549 cells. Fasudil, a selective ROCK inhibitor, showed similar effects. Overall, the findings indicate that AL suppresses the expression of messenger RNAs and proteins associated with Rho/ROCK/NF-κB signaling to effectively ameliorate lung injury. K E Y W O R D S alkannin, lipopolysaccharide, lung injury, Rho/ROCK/NF-κB

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Section: Discussionsupporting

confidence: 80%

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

Lin

Hou

et al. 2019

J Biochem & Molecular Tox

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“…A PID model in rats was established based on previously published protocols (13,14). Rats in the study were immediately administered intramuscular injections of buprenorphine (0.01 mg/kg; bid; Tianjin Medicine Research Institute Pharmaceutical Co., Ltd., Tianjin, China) to relieve pain following infection (17). All rats were acclimated for 7 days and subcutaneously injected with 45 mg/kg progesterone (Zhejiang Xianju Pharmaceutical Co., Ltd., Taizhou, China) prior to infection.…”

Section: Chemicals and Reagents Aa Was Purchased Frommentioning

confidence: 99%

“…AA inhibits neutrophil infiltration. MPO activity was assessed, as it is an oxidative enzyme in neutrophils and acts as a specific marker of neutrophil infiltration (16,17,21) (Fig. 2).…”

Section: Aa Reduces the Level Of Inflammatory Cytokines And Chemokinementioning

confidence: 99%

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Protective effects of Asiatic acid against pelvic inflammatory disease in rats

Kong

Fu²,

Zhang³

et al. 2019

Exp Ther Med

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Asiatic acid (AA) is one of the major components of the Chinese herb Centella asiatica and exerts a variety of pharmacological activities. However, the pharmacological effects of AA on pelvic inflammatory disease (PID) remain unknown. The purpose of the present study was to investigate the therapeutic efficacy and potential mechanisms of AA on PID in rats. A total of 75 female Sprague Dawley rats were randomly divided into the following five groups: A control group; a PID group; a PID + AA 5 mg/kg group; a PID + AA 35 mg/kg group; and a PID + AA 75 mg/kg group. Changes in cytokine and chemokine levels, myeloperoxidase (MPO) activity, nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome and nuclear factor-κB (NF-κB) activation, oxidative stress and cleaved caspase-3 were measured. AA treatment significantly decreased the excessive production of cytokines and chemokines and suppressed MPO activity and the activation of NLRP3 inflammasome, NF-κB and caspase-3, as well as oxidative stress. These results suggest that AA exhibits potent anti-inflammatory and antioxidant effects in rats with pathogen-induced PID and that the mechanism of these anti-inflammatory effects may be associated with the suppression of NLRP3 inflammasome activation and the NF-κB pathway.

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“…SCI not only results in inflammation of partial spinal cord tissue, but also induces systemic inflammatory response syndrome and secondary lung injury (Bao, Brown, Dekaban, Omana, & Weaver, ; Bao, Omana, Brown, & Weaver, ; W. Jiang, Li, He, Bian et al, ; W. Jiang, Li, He, Yao et al, ; Sun et al, ), which leads to the formation of susceptible environment of pulmonary infections and cause pulmonary dysfunction. Lung injury following SCI is crucial for the pathological basis of respiratory complications (He & Nan, ; Yong, Lili, Wen, Xinwei, & Xuhui, ).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of NLRP3 inflammasome attenuates spinal cord injury‐induced lung injury in mice

Jiang

et al. 2018

Journal Cellular Physiology

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Spinal cord injury (SCI) is one kind of severe traumatic injury, resulting in systemic inflammatory response syndrome and secondary lung injury, which is an important pathological basis of respiratory complications. The nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome is an important cytosolic protein complex in many inflammatory diseases. Hence, it is inescapable to explore the effect of inhibition of NLRP3 inflammasome by inhibitors in a mouse SCI model, which was conducted by using the method of 30-G closing force aneurysm clipping at T6-T7 spinal segment for 1 min, followed by assessment of edema, histology, alveolar type II cell apoptosis, mitochondrial dysfunction, and neutrophil infiltration. In brief, our results showed that, NLRP3 inflammasome inhibitor BAY 11-7082 or A438079 inhibited activation of NLRP3 inflammasome, alleviated mitochondrial dysfunction, the number of macrophage and neutrophil, thereby attenuating alveolar type II cell apoptosis, lung edema, and histological injury. Taken together, our data reveal that NLRP3 inflammasome inhibitor BAY 11-7082 or A438079 attenuates the inflammatory response, reverses mitochondrial dysfunction, and subsequently alleviates secondary lung injury following SCI.

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Protective Effects of Asiatic Acid Against Spinal Cord Injury-Induced Acute Lung Injury in Rats

Cited by 30 publications

References 42 publications

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

Protective effects of Asiatic acid against pelvic inflammatory disease in rats

Inhibition of NLRP3 inflammasome attenuates spinal cord injury‐induced lung injury in mice

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