Peitu Shengjin Recipe Attenuates Airway Inflammation via the TLR4/NF-kB Signaling Pathway on Chronic Obstructive Pulmonary Disease.

Background: Chronic obstructive pulmonary disease (COPD) is a common respiratory disease, but there is no specific medicine for COPD. In this study, we aimed to evaluate the effects of Peitu Shengjin Recipe (PSR) and Biostime Probiotic Powder on COPD rats. Methods: UPLC-Q/TOF-MS was used to detect the chemical constituents in PSR. The COPD rat model was established by cigarette smoke combined with tracheal injection of lipopolysaccharide. We assessed lung function by calculating FEV0.3/FVC%, dynamic lung compliance (Cdyn), and resistance of inspiration (RI). Histological analysis was performed by HE staining. The levels of TNF-α, IFN-γ, IL-1ß, IL-4, and IL-10 were detected by the ELISA. The mRNA and protein expressions of the TLR4/NF-kB signaling pathway were detected by the qRT-PCR and western blotting, respectively. Results: There were 53 ESI+ and 50 ESI- components in PSR. After high-dose PSR treatment, FEV0.3/FVC% and Cdyn increased significantly, while RI decreased. Compared with the COPD model, the RI of the Biostime Probiotic Powder group was significantly lower. HE staining showed that the inflammatory cell infiltration was reduced to varying degrees, the bronchial tube wall was not thickened, and the alveoli were relatively intact after treatment with PSR and Biostime Probiotic Powder. Compared with the model group, the levels of TNF-α, IFN-γ, IL-1ß, IL-4, and IL-10 in the PSR group and the Biostime Probiotic Powder group were reversed. The mRNA and protein expressions of TLR4 and NF-kB were significantly decreased after PSR and Biostime Probiotic Powder treatment. Conclusion: Our findings suggest that PSR and Biostime Probiotic Powder have protective effects on COPD rats, which may be achieved by modulating the TLR4/NF-kB signaling pathway.

Antagonism of scavenger receptor CD36 by 5A peptide prevents chronic kidney disease progression in mice independent of blood pressure regulation.

Scavenger receptor CD36 participates in lipid metabolism and inflammatory pathways important for cardiovascular disease and chronic kidney disease (CKD). Few pharmacological agents are available to slow the progression of CKD. However, apolipoprotein A-I-mimetic peptide 5A antagonizes CD36 in vitro. To test the efficacy of 5A, and to test the role of CD36 during CKD, we compared wild-type to CD36 knockout mice and wild-type mice treated with 5A, in a progressive CKD model that resembles human disease. Knockout and 5A-treated wild-type mice were protected from CKD progression without changes in blood pressure and had reductions in cardiovascular risk surrogate markers that are associated with CKD. Treatment with 5A did not further protect CD36 knockout mice from CKD progression, implicating CD36 as its main site of action. In a separate model of kidney fibrosis, 5A-treated wild-type mice had less macrophage infiltration and interstitial fibrosis. Peptide 5A exerted anti-inflammatory effects in the kidney and decreased renal expression of inflammasome genes. Thus, CD36 is a new therapeutic target for CKD and its associated cardiovascular risk factors. Peptide 5A may be a promising new agent to slow CKD progression.