Phloridzin reduces synovial hyperplasia and inflammation in rheumatoid arthritis rat by modulating mTOR pathway.

Rheumatoid arthritis (RA) is an inflammatory autoimmune disease and management of it still a challenge. Given report evaluates protective effect of phlorizin on RA and also postulates the molecular mechanism of its action. Bovine type II collagen (CIA) and Freund's incomplete adjuvant (1:1 and 1 mg/ml) was administered on 1st and 8th day of protocol to induce RA in rats and treatment with phlorizin 60 and 120 mg/kg was started after 4th week of protocol. Level of inflammatory cytokines and expression of proteins were estimated in phlorizin treated RA rats. Moreover in-vitro study was performed on Fibroblast-like synoviocytes (FLSs) and effect of phlorizin was estimated on proliferation, apoptosis and expression of mTOR pathway protein after stimulating these cell lines with Tumour Necrosis Factor alpha (TNF-α). Data of study suggest that phlorizin reduces inflammation and improves weight in CIA induced RA rats. Level of inflammatory cytokines in the serum and expression of Akt/PI3K/mTOR proteins in the join tissue was reduced in phlorizin treated RA rats. Phlorizin also reported to reverse the histopathological changes in the joint tissue of RA rats. In-vitro study supports that phlorizin reduces proliferation and no apoptotic effect on TNF-α stimulated FLSs. Expression of Akt/PI3K/mTOR proteins also downregulated in phlorizin treated TNF-α stimulated FLSs. In conclusion, phlorizin protects inflammation and reduces injury to the synovial tissues in RA, as it reduces autophagy by regulating Akt/PI3K/mTOR pathway.

Phlorizin Regulates Synovial Hyperplasia and Inflammation in Rats With Rheumatoid Arthritis by Regulating the mTOR Pathway.

BACKGROUND/AIM: Rheumatoid arthritis (RA) is an inflammatory autoimmune disease, and management of it is still a challenge. The present investigation assessed the potential preventive effect of phlorizin on rats with RA. MATERIALS AND METHODS: A total of 40 healthy Wistar rats were used for this study. Bovine type II collagen and Freund's incomplete adjuvant (1:1 and 1 mg/ml) were administered on days 1 and 8 of the protocol to induce RA in rats; treatment with phlorizin at 60 or 120 mg/kg was started after the 4th week of the protocol, and its effect on inflammation, level of inflammatory cytokines, and expression of proteins were estimated in RA rats. Moreover, an in vitro study was performed on fibroblast-like synoviocytes (FLSs), and the effects of phlorizin on proliferation, apoptosis, and expression of the mechanistic target of rapamycin kinase pathway protein after stimulating these cells with tumor necrosis factor α (TNF-α) were estimated. RESULTS: The data obtained from the study indicate that phlorizin has the potential to mitigate inflammation and enhance weight management in rats with RA induced by bovine type II collagen (CII). The level of inflammatory cytokines in the serum and the expression of protein kinase B (AKT), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), and mechanistic target of rapamycin kinase (mTOR) proteins in the joint tissue were reduced in phlorizin-treated rats with RA. In this investigation, phlorizin was shown to reverse the histological abnormalities in the joint tissue of rats with RA. The in-vitro study showed that phlorizin reduced proliferation and had no apoptotic effect on TNF-α-stimulated FLSs. Expression of AKT, PI3K, and mTOR proteins was also down-regulated in phlorizin-treated TNF-α-stimulated FLSs. CONCLUSION: Phlorizin protects against inflammation and reduces injury to synovial tissues in RA by modulating the AKT/PI3K/mTOR pathway.

Spatial-Temporal Characteristics and Influence Factors of Carbon Emission from Livestock Industry in China.

Animal husbandry is an important source of carbon emissions. As a large country, China must measure the carbon emissions from animal husbandry to reveal the spatial and temporal characteristics and determine the influencing factors to realize low-carbon animal husbandry and carbon emission reduction. In this paper, the carbon emissions of the livestock industry in each province of China were calculated with the emission coefficient method, considering the temperature change factor. The spatial and temporal characteristics and influencing factors of livestock industry carbon emissions were analyzed using the kernel density model, the spatial autocorrelation model, and the Tobit model. The results indicated that: (1) From 2000 to 2020, carbon emissions from the livestock industry in China experienced four stages: rapid rise, rapid decline, slow rise, and fluctuating decline, with an overall downward trend. Carbon emissions in the eastern and central regions showed a downward trend, while carbon emissions in the western regions showed an upward trend. (2) In terms of time, the relative gap in carbon emissions among the provinces narrowed first and then widened; the spatial agglomeration of carbon emissions from livestock farming in China increased, gradually forming the characteristics of "high agglomeration, low agglomeration", and showing a gradually decreasing pattern from northwest to southeast. (3) Nationwide, industrial structure, population, and farmers' income levels have had significantly promoting effects on animal husbandry carbon emissions, and the urbanization and agricultural mechanization levels have had significant inhibitory effects on carbon emissions. Finally, based on the above factors, it can be concluded that recognizing the location conditions, promoting the upgrading of industrial structures, and adopting differentiated strategies will help to promote the reduction in carbon emissions in animal husbandry and achieve its high-quality development.