Soy isoflavone reduces LPS-induced acute lung injury via increasing aquaporin 1 and aquaporin 5 in rats

Abstract

Acute lung injury (ALI) followed with severe inflammation and oxidative stress. Anti-inflammatory and antioxidant are the properties of aquaporin 1 (AQP1) and aquaporin 5 (AQP5). The goal of this study was to see if soy isoflavone can diminish lipopolysaccharide (LPS)-induced ALI and the underling mechanism. LPS-induced ALI was given to Sprague–Dawley rats 14 days following oophorectomy. One hour before the LPS challenge, estradiol (1 mg/kg) was administered subcutaneously as positive control and soy isoflavone was intragastric administration for 14 days prior to LPS challenge with different doses. Six hours after LPS challenge, the pulmonary edema, pathophysiology, inflammation, and the oxidative stress in lung tissues of rats were discovered. We found that soy isoflavone can reduce pulmonary edema and the lung pathology in a dose-dependent manner. Furthermore, tumor necrosis factor-alpha, interleukin-1β, and interleukin-6 were decreased in rats treated with soy isoflavone. Meanwhile, soy isoflavone reduced pulmonary oxidative stress by decreasing malondialdehyde levels, while increasing superoxide dismutase levels in lung tissues in a dose-dependent manner. Mechanically, we found that the mRNA and protein level of AQP1 and AOP5 were increased in lung tissues of rats treated with soy isoflavone compared the LPS-treated rats. Thus, soy isoflavone alleviates LPS-induced ALI through inducing AQP1 and AQP5.

Secretion of related factors and AMPK/PGC-1 α signal pathway by alveolar macrophages in viral acute lung injury

“…In addition, it has been found that apoptosis of alveolar macrophages is an important link in the VALI progression. In many cases, such as endogenous or exogenous stimulation, alveolar macrophages can be induced to enter the apoptosis process (18). The increase in the number of apoptosis of alveolar macrophages not only leads to the non-phagocytosis of apoptotic neutrophils but also causes the release of inflammatory mediators and oxidative stress-related products to of the VALIG were reduced than that of the BCG(P<0.05) (Table 4).…”

Aquaporin Expression and Regulation in Clinical and Experimental Sepsis

“…Pre-treatment of rats with increasing concentrations of soy isoflavone resulted in a dose-dependent upregulation of AQP1 and AQP5 mRNA and protein expression. Additionally, soy isoflavone was found to decrease TNF-α, IL-1β, and IL-6 levels, alleviating pulmonary edema and lung damage [ 37 ].…”

“…Table 3 lists the regulators of AQP expression and their effects on experimental sepsis progression. LPS-exposed rats Pre-treatment with increasing concentrations of soy isoflavone resulted in dose-dependent upregulation of AQP1 mRNA and protein, alleviating pulmonary edema and lung damage [37] LPS-exposed rats Hydrogen-rich saline reverses AQP1 mRNA and protein downregulation [38] LPS-exposed rats Selenium treatment resulted in the upregulation of AQP1 protein expression in the kidneys [39] CLP rats MEF2C treatment attenuated the progress of lung injury while upregulating AQP1 mRNA and protein expression [40] CLP rats Emodin pre-treatment significantly increased AQP1 mRNA and protein expression, suppressing sepsis-induced pulmonary apoptosis [26] LPS-exposed HPMECs Silencing HIF1A expression in LPS-induced cells attenuated AQP1 upregulation and regulated the cells' volume increase [41] AQP2 LPS-exposed rats Dexpanthenol increased AQP2 mRNA expression in kidney tissues through the SIRT1 signaling pathway [43] LPS-exposed rats Rhein treatment attenuated the downregulation of AQP2 protein expression in the kidneys [42] LPS-exposed rats Propofol pre-treatment protected the rats from further kidney complications by restoring AQP2 mRNA levels [44] AQP3 CLP rats Ss-31 treatment resulted in decreased protein expression of AQP3 and pulmonary vascular permeability [27] AQP4 LPS-exposed mice TGN-020 treatment resulted in downregulation of AQP4, suppression of inflammatory cytokine production, and better survival rates [75] AQP5 LPS-exposed mice Lipoxin A 4 presents a protective role in lung injury by upregulating AQP5 protein expression in lung tissue [47] LPS-exposed mice Fasudil upregulates AQP5 mRNA and protein levels while eliminating LPS-induced lung edema and preventing LPS-induced pulmonary inflammation [46] LPS-exposed mice Estradiol treatment pre-LPS exposure upregulated AQP5 mRNA and protein levels, reducing oxidative stress and inflammatory responses [36] LPS-exposed rats Hydrogen-rich saline reverses AQP5 mRNA and protein downregulation [38] LPS-exposed rats Pre-treatment with increasing concentrations of soy isoflavone resulted in dose-dependent upregulation of AQP5 mRNA and protein, alleviating pulmonary edema and lung damage [37] CLP rats…”

Early Endothelial Signaling Transduction in Developing Lung Edema

“…At the therapeutic level, an interesting report focuses on the role of ropivacaine to inhibit/prevent pressure-induced lung endothelial hyperpermeability [ 73 ]. Further, soy isoflavone has been proposed to reduce pulmonary edema in a dose-dependent manner [ 74 ]. Mesenchymal stem cell therapies are also reported as promising therapeutic agents in ARDS [ 75 ].…”