scholarly journals Salvianolic Acid B Improves the Effect of Fat Grafts by Inhibiting the NF-kB Signalling Pathway in Macrophages

2021 ◽  
Author(s):  
Jia-Ming Sun ◽  
Chia-Kang Ho ◽  
Ya Gao ◽  
Chio-Hou Chong ◽  
Yang-Dan Liu ◽  
...  
Keyword(s):  
Graft Survival ◽  
Salvia Miltiorrhiza ◽  
Salvianolic Acid B ◽  
Raw264.7 Cells ◽  
Fat Transplantation ◽  
Salvianolic Acid ◽  
Fat Grafts ◽  
Anti Inflammatory

Abstract Background Autologous fat grafting (AFG), although an appealing approach to repair soft tissue defects, has various complications. Excessive inflammation at the transplant site is one of the main reasons for the poor effect of fat transplantation and occurrence of complications. Our previous study proved that Salvia miltiorrhiza can enhance fat graft survival. Salvianolic acid B (Sal-B) is the most abundant and bioactive water-soluble compound in Salvia miltiorrhiza and has anti-inflammatory effects on other diseases. Therefore, we hypothesized that salvianolic acid B could improve the effect of fat grafts by inhibiting inflammation. Methods In vivo, 0.2 ml of Coleman fat was transplanted into nude mice with salvianolic acid B. The grafts were evaluated by HE and IF at 2, 4 and 12 weeks posttransplantation and by micro-CT at 4 weeks posttransplantation. In vitro, the proliferative and anti-inflammatory activities of salvianolic acid B were analyzed in cultured RAW264.7 cells to detect the mechanism by which salvianolic acid B affects graft survival by inhibiting inflammation. Results In vivo, the degree of adipose tissue fibrosis and inflammatory cell infiltration in the salvianolic acid B treatment group was lower, and the infiltration of M1 macrophages in fat grafts was also less than that in the control group. In vitro, salvianolic acid B inhibited the proliferation and activation of inflammatory pathways in RAW264.7 cells. Conclusions This study demonstrates the use of salvianolic acid B as a possible treatment to improve the effect of fat transplantation.

scholarly journals Salvianolic acid-B improves fat graft survival by promoting proliferation and adipogenesis

2021 ◽  
Author(s):  
Jia-Ming Sun ◽  
Chia-Kang Ho ◽  
Ya Gao ◽  
Chio-Hou Chong ◽  
Dan-Ning Zheng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Graft Survival ◽  
Salvia Miltiorrhiza ◽  
Salvianolic Acid B ◽  
Fat Graft ◽  
Fat Transplantation ◽  
Salvianolic Acid ◽  
Fat Grafts

Abstract Background: Our previous study proved that Salvia miltiorrhiza could enhance fat graft survival by promoting adipogenesis. However, the effect of salvianolic acid B (Sal-B), the most abundant and bioactive water-soluble compound in Salvia miltiorrhiza, on fat graft survival has not yet been investigated.Objective: This study aims to investigate whether salvianolic acid B could improve fat graft survival and promote preadipocyte differentiation. The underlying mechanism has also been studied.Methods: In vivo, 0.2 ml of Coleman fat was transplanted into nude mice with salvianolic acid B. The grafts were evaluated by HE and IF at 2 and 4 weeks posttransplantation and by micro-CT at 4 weeks posttransplantation. In vitro, the adipogenesis and proliferative activities of salvianolic acid B were analyzed in cultured human adipose-derived stem cells (h-ADSCs) and 3T3-L1 cells to detect the mechanism by which salvianolic acid B affects graft survival.Results: In vivo, the weights and volumes of the fat grafts in the Sal-B-treated groups were significantly higher than those of the fat grafts in the control group. In addition, higher fat integrity and more viable adipocytes were observed in the Sal-B-treated groups. In vitro, salvianolic acid B showed the ability to promote 3T3-L1 and h-ADSC proliferation and adipogenesis.Conclusions: Our in vitro experiments demonstrated that salvianolic acid B can promote the proliferation of adipose stem cells and enhance the differentiation of adipose stem cells. Simultaneously, in vivo experiments showed that salvianolic acid B can improve the survival rate of fat transplantation. Therefore, our research shed light on the potential therapeutic usage of salvianolic acid B in improving the survival rate of fat transplantation.

scholarly journals Salvianolic acid-B improves fat graft survival by promoting proliferation and adipogenesis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jia-Ming Sun ◽  
Chia-Kang Ho ◽  
Ya Gao ◽  
Chio-Hou Chong ◽  
Dan-Ning Zheng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Graft Survival ◽  
Salvia Miltiorrhiza ◽  
Salvianolic Acid B ◽  
Fat Graft ◽  
Fat Transplantation ◽  
Salvianolic Acid ◽  
Fat Grafts

Abstract Background Our previous study proved that Salvia miltiorrhiza could enhance fat graft survival by promoting adipogenesis. However, the effect of salvianolic acid B (Sal-B), the most abundant and bioactive water-soluble compound in Salvia miltiorrhiza, on fat graft survival has not yet been investigated. Objective This study aims to investigate whether salvianolic acid B could improve fat graft survival and promote preadipocyte differentiation. The underlying mechanism has also been studied. Methods In vivo, 0.2 ml of Coleman fat was transplanted into nude mice with salvianolic acid B. The grafts were evaluated by HE and IF at 2 and 4 weeks posttransplantation and by micro-CT at 4 weeks posttransplantation. In vitro, the adipogenesis and proliferative activities of salvianolic acid B were analyzed in cultured human adipose-derived stem cells (h-ADSCs) and 3T3-L1 cells to detect the mechanism by which salvianolic acid B affects graft survival. Results In vivo, the weights and volumes of the fat grafts in the Sal-B-treated groups were significantly higher than those of the fat grafts in the control group. In addition, higher fat integrity and more viable adipocytes were observed in the Sal-B-treated groups. In vitro, salvianolic acid B showed the ability to promote 3T3-L1 and h-ADSC proliferation and adipogenesis. Conclusions Our in vitro experiments demonstrated that salvianolic acid B can promote the proliferation of adipose stem cells and enhance the differentiation of adipose stem cells. Simultaneously, in vivo experiments showed that salvianolic acid B can improve the survival rate of fat transplantation. Therefore, our research shed light on the potential therapeutic usage of salvianolic acid B in improving the survival rate of fat transplantation.

Ulinastatin Activated The ERK5/Mer Signaling Pathway To Promote Macrophage Efferocytosis And Ameliorate Lung Inflammation

2021 ◽  
Author(s):  
Jinju Li ◽  
Rongge Shao ◽  
Qiuwen Xie ◽  
XueKe Du
Keyword(s):  
Lung Injury ◽  
Signaling Pathway ◽  
Lung Inflammation ◽  
Raw264.7 Cells ◽  
Inflammatory Factors ◽  
Inflammatory Factor ◽  
Dependent Manner ◽  
Anti Inflammatory

Abstract Purpose:Ulinastatin (UTI) is an endogenous protease inhibitor with potent anti-inflammatory, antioxidant and organ protective effects. The inhibitor has been reported to ameliorate inflammatory lung injury but precise mechanisms remain unclear. Methods: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). The number of neutrophils and the phagocytosis of apoptotic neutrophils were observed by Diff- Quick method. Lung injury was observed by HE staining .BALF cells were counted by hemocytometer and concentrations of protein plus inflammatory factors were measured with a BCA test kit. During in vitro experiments, RAW264.7 cells were pretreated with UTI (1000 and 5000U/ mL), stained with CellTrackerTM Green B0DIPYTM and HL60 cells added with UV-induced apoptosis and PKH26 Red staining. The expression of ERK5\Mer related proteins was detected by western blot and immunofluorescence.Results: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). UTI treatment enhanced the phagocytotic effect of mouse alveolar macrophages on neutrophils, alleviated lung lesions, decreased the pro-inflammatory factor and total protein content of BALF and increased levels of anti-inflammatory factors. in vitro experiments ，UTI enhanced the phagocytosis of apoptotic bodies by RAW264.7 cells in a dose-dependent manner. Increased expression levels of ERK5 and Mer by UTI were shown by Western blotting and immunofluorescence.Conclusions: UTI mediated the activation of the ERK5/Mer signaling pathway, enhanced phagocytosis of neutrophils by macrophages and improved lung inflammation. The current study indicates potential new clinical approaches for accelerating the recovery from lung inflammation.

Salvianolic acid B exerts anti-liver fibrosis effects via inhibition of MAPK-mediated phospho-Smad2/3 at linker regions in vivo and in vitro

Life Sciences ◽  
2019 ◽  
Vol 239 ◽  
pp. 116881 ◽  
Author(s):  
Chao Wu ◽  
Weiyang Chen ◽  
Hanyan Ding ◽  
Dong Li ◽  
Guanghua Wen ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Salvianolic Acid B ◽  
Salvianolic Acid

scholarly journals Impact of Sodium N-[8-(2-Hydroxybenzoyl)amino]-caprylate on Intestinal Permeability for Notoginsenoside R1 and Salvianolic Acids in Caco-2 Cells Transport and Rat Pharmacokinetics

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2990 ◽  
Author(s):  
Ying Li ◽  
Dandan Yang ◽  
Chunyan Zhu
Keyword(s):  
Membrane Permeability ◽  
Cell Monolayer ◽  
Salvianolic Acid B ◽  
Absorption Enhancement ◽  
Enhancement Effect ◽  
Absorption Enhancers ◽  
Salvianolic Acid ◽  
Salvianolic Acids

For drugs with high hydrophilicity and poor membrane permeability, absorption enhancers can promote membrane permeability and improve oral bioavailability. Sodium N-[8-(2-hydroxybenzoyl)amino]caprylate (SNAC) is a new kind of absorption enhancer that has good safety. To investigate the absorption enhancement effect of SNAC on non-polar charged and polar charged drugs and establish the absorption enhancement mechanism of SNAC, SNAC was synthesized and characterized. Two representative hydrophilic drugs—notoginsenoside R1 (R1) and salvianolic acids (SAs)—were selected as model drugs. In vitro Caco-2 cells transport and in vivo rat pharmacokinetics studies were conducted to examine the permeation effect of SNAC on R1 and SAs. R1, rosmarinic acid (RA), salvianolic acid B (SA-B) and salvianolic acid B (SA-A) were determined to compare the permeation enhancement of different drugs. The MTT assay results showed that SNAC had no toxicity to Caco-2 cells. The transepithelial electrical resistance (TEER) of Caco-2 cell monolayer displayed that SNAC facilitated passive transport of polar charged SAs through the membrane of epithelial enterocytes. The pharmacokinetics results demonstrated that area under the curve (AUC) of RA, SA-B and SA-A with administration of SAs containing SNAC was 35.27, 8.72 and 9.23 times than administration of SAs. Tmax of RA, SA-B and SA-A were also prolonged. The AUC of R1 with administration of R1 containing SNAC was 2.24-times than administration of R1. SNAC is more effective in promoting absorption of SAs than R1. The study demonstrated that SNAC significantly improved bioavailability of R1 and SAs. What’s more, the effect of SNAC on absorption enhancement of charged drugs was larger than that of non-charged drugs. The current findings not only confirm the usefulness of SNAC for the improved delivery of R1 and SAs but also demonstrate the importance of biopharmaceutics characterization in the dosage form development of drugs.

scholarly journals Dual Effect of Soloxolone Methyl on LPS-Induced Inflammation In Vitro and In Vivo

2020 ◽  
Vol 21 (21) ◽  
pp. 7876
Author(s):  
Andrey V. Markov ◽  
Aleksandra V. Sen’kova ◽  
Valeriya O. Babich ◽  
Kirill V. Odarenko ◽  
Vadim A. Talyshev ◽  
...  
Keyword(s):  
Acute Inflammation ◽  
Nuclear Factor Κb ◽  
Raw264.7 Cells ◽  
Migration Activity ◽  
Akt Phosphorylation ◽  
Raw264.7 Macrophages ◽  
Anti Inflammatory ◽  
And Migration

Plant-extracted triterpenoids belong to a class of bioactive compounds with pleotropic functions, including antioxidant, anti-cancer, and anti-inflammatory effects. In this work, we investigated the anti-inflammatory and anti-oxidative activities of a semisynthetic derivative of 18βH-glycyrrhetinic acid (18βH-GA), soloxolone methyl (methyl 2-cyano-3,12-dioxo-18βH-olean-9(11),1(2)-dien-30-oate, or SM) in vitro on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and in vivo in models of acute inflammation: LPS-induced endotoxemia and carrageenan-induced peritonitis. SM used at non-cytotoxic concentrations was found to attenuate the production of reactive oxygen species and nitric oxide (II) and increase the level of reduced glutathione production by LPS-stimulated RAW264.7 cells. Moreover, SM strongly suppressed the phagocytic and migration activity of activated macrophages. These effects were found to be associated with the stimulation of heme oxigenase-1 (HO-1) expression, as well as with the inhibition of nuclear factor-κB (NF-κB) and Akt phosphorylation. Surprisingly, it was found that SM significantly enhanced LPS-induced expression of the pro-inflammatory cytokines interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in RAW264.7 cells via activation of the c-Jun/Toll-like receptor 4 (TLR4) signaling axis. In vivo pre-exposure treatment with SM effectively inhibited the development of carrageenan-induced acute inflammation in the peritoneal cavity, but it did not improve LPS-induced inflammation in the endotoxemia model.

Analysis on the Stability of Total Phenolic Acids and Salvianolic Acid B from Salvia miltiorrhiza by HPLC and HPLC-MSn

2008 ◽  
Vol 3 (5) ◽  
pp. 1934578X0800300 ◽  
Author(s):  
Man Xu ◽  
Jian Han ◽  
Hui-feng Li ◽  
Li Fan ◽  
Ai-hua Liu ◽  
...  
Keyword(s):  
Phenolic Acids ◽  
Degradation Products ◽  
Biological Fluids ◽  
Salvia Miltiorrhiza ◽  
Degradation Pathway ◽  
Salvianolic Acid B ◽  
Total Phenolic ◽  
Salvianolic Acid ◽  
The Stability

The stability of salvianolic acid B and total phenolic acids from Salvia miltiorrhiza in water solutions at different temperatures, in buffered aqueous solutions at different pHs and in biological fluids, including simulated gastric and intestinal fluids, were investigated in vitro. The results showed that the degradation of salvianolic acid B was pH- and temperature-dependent. Furthermore, structures of the degradation products of salvianolic acid B and total phenolic acids were elucidated by liquid chromatography-electrospray ion trap mass spectrometry and analysis of the degraded solutions revealed seventeen degradation products. The possible degradation pathway of salvianolic acid B is proposed.

scholarly journals Wnt/β-catenin signaling regulates lipopolysaccharide-altered polarizations of RAW264.7 cells and alveolar macrophages in mouse lungs

2021 ◽  
Vol 19 ◽  
pp. 205873922110593
Author(s):  
Jiali Yang ◽  
Ying Wang ◽  
Dandan Yang ◽  
Jia Ma ◽  
Shuang Wu ◽  
...  
Keyword(s):  
Alveolar Macrophage ◽  
Alveolar Macrophages ◽  
Macrophage Polarization ◽  
Raw264.7 Cells ◽  
M1 Polarization ◽  
Inflammatory Phenotype ◽  
Inflammatory State ◽  
Anti Inflammatory

Introduction Macrophages are capable of exerting both proinflammatory and anti-inflammatory functions in response to distinct environmental stimuli, by polarizing into classically inflammatory state (M1) and anti-inflammatory phenotype (M2), respectively. The Wnt/β-catenin signaling plays an important role in the tissue homeostasis and immune regulations, including the macrophage polarizations. However, the molecular mechanism of Wnt/β-catenin signaling in regulating alveolar macrophage polarization in an inflammatory state remains unclear. Methods The Wnt/β-catenin signaling-altered phenotypes of murine macrophage-like RAW264.7 cells in vitro and alveolar macrophage in vivo in both of naïve and lipopolysaccharide-induced inflammation states were accessed by immunoblotting and immunostaining assays. Results The activation of Wnt/β-catenin signaling inhibited macrophage M1 polarization, but promoted alternative M2 polarization in murine RAW264.7 cells under a naïve state. Interestingly, in an LPS-induced inflammation condition, the enhanced Wnt/β-catenin activity suppressed both M1 and M2 polarizations in RAW264.7 cells in vitro, and primary alveolar macrophages of LPS-challenged mice in vivo. Molecular analysis further demonstrated an involvement of Stat signing in regulating Wnt/β-catenin signaling-altered polarizations in mouse alveolar macrophages. Conclusion These results suggest a mechanism by which Wnt/β-catenin signaling modulates macrophage polarization in an inflammation state by regulating the Stat signaling pathway.

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