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. 2020 Sep 23;11:522729. doi: 10.3389/fphar.2020.522729

Figure 5.

Figure 5

Lian Hua Qing Wen capsule (LHQW) specifically inhibited endoplasmic reticulum stress (ERS) through c-Jun N-terminal kinase (JNK) pathway activation. Bronchoalveolar lavage fluid (BALF) samples were centrifuged, and pulmonary macrophages were isolated with the adherent method. THP1 cells were first induced by PMA to differentiate into macrophages, and subsequently treated with LHQW and LPS for another 24 h. RAW 264.7 cells were also treated with LHQW and LPS for 24 h. (Togno-Peirce et al., 2013). In the cells, (A, B) LHQW enhanced SOCS3 expression in (A) THP1 cells, (B) RAW 264.7 cells by utilizing western blot. (C) LHQW decreased phospho-JNK expression by western blot analysis. In the tissues, (D) LHQW enhanced the translation of SOCS3 in alveolar macrophages. The data was presented as the mean ± S.E.M. of three independent experiments. # P < 0.05 vs. the NC group. * P < 0.05, ** P < 0.01 vs. the LPS group. LHQW-L: 50 μg/ml; LHQW-M: 100 μg/ml; LHQW-H: 500 μg/ml; TM, tunicamycin.