Anti-inflammatory activity of Sanghuangporus sanghuang by suppressing the TLR4-mediated PI3K/AKT/mTOR/IKKβ signaling pathway

Abstract

Sanghuangporus sanghuang (SS) is a mushroom that belongs to the genus Sanghuangporus and it is commonly called "Sangwhang" in Taiwan. It is popular in oriental countries and has been traditionally used as food and medicine. The mystery surrounding it was solved in 2012, when it was discovered. However, existing research has not extensively investigated the anti-inflammatory effect of sanghuang that grows on Morus trees. The aim of this study is to investigate the protective effects and underlying mechanism of SS on inflammation by lipopolysaccharide (LPS) induced in vitro and in vivo. Results showed that SS treatment markedly attenuated LPS-induced lung edema, by elevation of the levels of interleukin (IL)-1b, tumor necrosis factor (TNF)-a and IL-6 in bronchoalveolar lavage fluid (BALF) accompanied by a remarkable improvement of lung histopathological symptoms. Additionally, western blotting results suggest that anti-inflammatory effects of SS against the LPS-induced ALI may be due to its ability to inhibit the PI3K/Akt/mTOR/IKK, NF-kB and MAPK signaling pathways. Notably, our results suggest that SS suppresses LPS-induced ROS by inducing Nrf2 activation and HO-1, thioredoxin-1 expression in the lung tissues. Moreover, these findings suggest a potential application of SS in pulmonary inflammatory disease therapy.

Cordyceps cicadae Mycelia Ameliorate Cisplatin-Induced Acute Kidney Injury by Suppressing the TLR4/NF-κB/MAPK and Activating the HO-1/Nrf2 and Sirt-1/AMPK Pathways in Mice

“…Incorporation of DCFH-DA into cells leads to its conversion to 2,7-dichlorofluorescein (DCF) by oxidative processes. RAW264.7 cells were incubated with or without samples and then continuously stimulated with LPS (100 ng/mL) for 24 h. After washing thrice with phosphate-buffered saline, the cells were treated with serum-free medium containing 10 μM H 2 DCFDA (Invitrogen, Carlsbad, CA, USA) for 30 min at 37°C in the dark and washed again with phosphate-buffered saline three times; then, the DCF fluorescence was detected by using a Synergy HT Microplate Reader (BioTek Instruments) with an excitation wavelength of 485 nm and emission wavelength of 535 nm [24].…”

The role of TLR-4 in the immunomodulatory effects of recombinant BCG expressing MSP-1C of Plasmodium falciparum

“…Further analysis showed that the increases in iNOS and NO were both significantly inhibited in the presence of TAK-242. Previous studies by others also showed that the inhibition of TLR-4 led to the inhibition of LPS [20] and megalo-type α-1,6-glucosaccharideinduced NO production [21]. TLR-4 inhibition also decreased immunoexpression of iNOS in the microglia of day old Wistar rats [22] and allografts [23].…”

Ginsenoside Rh2 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury by Regulating the TLR4/PI3K/Akt/mTOR, Raf-1/MEK/ERK, and Keap1/Nrf2/HO-1 Signaling Pathways in Mice

“…Neutrophil infiltration can increase inflammatory responses and cell injury. However, MPO activity is a more useful index of neutrophil influx into lung tissue [ 18 ]. As Figure 2 B illustrates, mice were exposed to a significant increase in MPO activity via intratracheal instillation of LPS in lung tissues.…”

“…Therefore, suppression of inflammatory response could be a potential strategy to treat LPS-induced lung injury. GRh2 has been reported to attenuate allergic airway inflammation through an anti-inflammatory mechanism [ 18 ], but its effect on ALI is poorly understood. Thus, we found that GRh2 treatment reduced LPS-induced lung edema, neutrophil infiltration, secretion of proinflammatory cytokines in the BALF, and regulation of the Raf-1/MEK/ERK and Keap1/Nrf2/HO-1 signaling pathways.…”

“…Under oxidative stress, Nrf2 is released from Keap1, which activates Nrf2 and its downstream-regulated genes in the nucleus. Nrf2 is correlated with the induction of HO-1, GPx, glutathione-S-transferase, and Trx-1, allowing the scavenging of free radicals in cells caused by oxidative damage [ 18 ]. Nrf2 functions to maintain cellular homeostasis through its ability to regulate antioxidant proteins, detoxification enzymes, and other stress-response proteins [ 18 ].…”