Photobiomodulation reduces neutrophil migration and oxidative stress in mice with carrageenan-induced peritonitis

Costa, Mariana de Souza; Teles, Ramon Handerson Gomes; Dutra, Yago Medeiros; Neto, José Carlos Rapozo Mazulo; Brito, Tarcísio Vieira de; Queiroz, Francisca Francisete de Sousa Nunes; Vale, Donária Bezerra Nobre do; Souza, Luan Kelves Miranda de; Silva, Irismara Sousa; Barbosa, André Luiz dos Reis; Medeiros, Jand‐Venes Rolim; Parizotto, Nivaldo Antônio; Filgueiras, Marcelo de Carvalho

doi:10.1007/s10103-018-2569-7

Cited by 13 publications

(4 citation statements)

References 40 publications

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“…The use of carrageenan as an inflammatory inducer was shown in studies by de Souza et al [ 47 ], which demonstrated the capacity of carrageenan to generate an inflammatory response in rat and mouse paws. Moreover, carrageenan is frequently used in experimental models for the induction of peritonitis [ 48 , 49 ]. The molecules 8h , 12 , 5e , 9i , and 11 (0.1 mg/kg) reduced the recruitment of cells into the peritoneum when compared to control treatment, indicating that they can decrease the inflammatory process in vivo [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Triazoles with inhibitory action on P2X7R impaired the acute inflammatory response in vivo and modulated the hemostatic balance in vitro and ex vivo

et al. 2022

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Objective The present study aimed to investigate five triazole compounds as P2X7R inhibitors and evaluate their ability to reduce acute inflammation in vivo. Material The synthetic compounds were labeled 5e , 8h , 9i , 11 , and 12 . Treatment We administered 500 ng/kg triazole analogs in vivo, (1–10 µM) in vitro, and 1000 mg/kg for toxicological assays. Methods For this, we used in vitro experiments, such as platelet aggregation, in vivo experiments of paw edema and peritonitis in mice, and in silico experiments. Results The tested substances 5e , 8h , 9i , 11 , and 12 produced a significant reduction in paw edema. Molecules 5e , 8h , 9i , 11 , and 12 inhibited carrageenan-induced peritonitis. Substances 5e , 8h , 9i , 11 , and 12 showed an anticoagulant effect, and 5e at a concentration of 10 µM acted as a procoagulant. All derivatives, except for 11 , had pharmacokinetic, physicochemical, and toxicological properties suitable for substances that are candidates for new drugs. In addition, the ADMET risk assessment shows that derivatives 8h , 11 , 5e , and 9i have high pharmacological potential. Finally, docking tests indicated that the derivatives have binding energies comparable to the reference antagonist with a competitive inhibition profile. Conclusions Together, the results indicate that the molecules tested as antagonist drugs of P2X7R had anti-inflammatory action against the acute inflammatory response. Supplementary Information The online version contains supplementary material available at 10.1007/s00011-022-01664-1.

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Section: Discussionmentioning

confidence: 99%

Triazoles with inhibitory action on P2X7R impaired the acute inflammatory response in vivo and modulated the hemostatic balance in vitro and ex vivo

et al. 2022

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“…Accumulating evidence indicates that κ-CGNs, especially their low-MW degradation products, induce inflammation in the colon, resulting in a range of diseases in cell and animal models, including thrombosis [28][29][30][31], peritonitis [26,[32][33][34], paw edema [35,36], pleurisy [37,38], gastroenterocolitis [39,40], arthritis [41,42], and inflammatory bowel disease. However, CGNs also show positive health effects, such as antitumor [43], antimicrobial [44], and antiviral [45,46].…”

Section: Discussionmentioning

confidence: 99%

Carrageenan oligosaccharides and their degrading bacteria induce intestinal inflammation in germ-free mouse

Yin

et al. 2020

Preprint

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Background: Carrageenans (CGNs) are widely used in food and pharmaceutical industries. However, the safety of CGNs is still under debate, because degraded CGNs have been reported to promote an intestinal inflammatory response in animal models. Here, we studied the relationship among CGNs, human gut microbiota, and the host inflammatory response.Methods: TLC was selected for detecting the degradation of KCPs by human gut microbiota in vitro batch fermentation system. PCR-DGGE and real time PCR were used for studying bacterial community. ESI-MS was used for KCPs structure analysis. Hematoxylin-eosin staining (HE), immunohistochemistry (IHC) and RNA-seq were used to evaluated the KCPs on host inflammation response in germ-free mice.Results: Thin-layer chromatography (TLC) data showed that CGNs with a molecular weight (Mw) higher than 100 kDa are not degraded by human fecal microbiota, but low Mw CGNs with an Mw around ~4.5 kDa (KCOs) could be degraded by seven of eight human fecal microbiota samples. KCO degrading B. xylanisolvens was isolated from fecal samples, and PCR-DGGE profiling with band sequencing suggested that B. xylanisolvens was the key KCO degrader in the human gut. Two putative κ-carrageenase genes were identified in the genome sequence of B. xylanisolvens. However, their function on KCO degrading was not verified in vitro. And the sulfate group from KCO is not removed after in vitro degradation by human fecal microbiota, as shown by ESI-MS analysis. The effects of KCO and KCO degrading bacteria on the inflammatory response were investigated in germ-free mice. Increased numbers of P-P38-, CD3a-, and CD79a-positive cells were found in the colon and rectum in mice fed with KCO plus KCO degrading bacteria than in mice fed with only KCO or only B. xylanisolvens and E. coli, as shown by RNA-Seq analysis, HE staining, and IHC. Conclusion: Our data suggested that the presence of KCO degrading bacteria promote the pro-inflammatory effects of CGNs.

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“…Control groups received PBS and carrageenan. The supernatants obtained from the peritoneal fluid were collected after four hours (de Souza Costa et al 2018). The levels of chemokine CXCL1 were measured by enzyme-linked immunosorbent assay (ELISA) using a commercially available ELISA DuoSet kit (R&D Systems, Minnesota, USA), in accordance with the manufacturer's instructions.…”

Section: Chemokine Levelsmentioning

confidence: 99%

Caryocar villosum attenuates inflammation by inhibiting CXCL1 activation and peripheral hyperalgesia through opioid pathway modulation

et al. 2022

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The oil of Caryocar villosum is used in Amazonian folk medicine to treat pain and inflammatory conditions. So, we assessed the anti-inflammatory and antinociceptive properties of the ethanolic extract obtained from the fruit peels of this species. The acetic acid-induced writhing, carrageenan-induced mechanical hyperalgesia, formalin, carrageenan-induced paw edema and carrageenan-induced peritonitis tests were used on mice. The C. villosum ethanolic extract significantly inhibited the number of abdominal writhes, mechanical hyperalgesia and paw licking time in the second phase of the formalin test. At a dose of 300 mg kg-1, the extract also significantly reduced the volume of edema formed in the late phase and reduced the recruitment of leukocytes and neutrophils in the peritoneal cavity, as well as CXCL1 chemokine levels. It is suggested that the extract attenuates the leukocyte recruitment by inhibiting the CXCL1 activation. The peripheral antinociceptive activity occured through opioid pathway modulation because pretreatment with C. villosum ethanolic extract reversed the naltrexone-induced antinociception.

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Photobiomodulation reduces neutrophil migration and oxidative stress in mice with carrageenan-induced peritonitis

Cited by 13 publications

References 40 publications

Triazoles with inhibitory action on P2X7R impaired the acute inflammatory response in vivo and modulated the hemostatic balance in vitro and ex vivo

Triazoles with inhibitory action on P2X7R impaired the acute inflammatory response in vivo and modulated the hemostatic balance in vitro and ex vivo

Carrageenan oligosaccharides and their degrading bacteria induce intestinal inflammation in germ-free mouse

Caryocar villosum attenuates inflammation by inhibiting CXCL1 activation and peripheral hyperalgesia through opioid pathway modulation

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