記述言語：英語   掲載種別：研究論文（学術雑誌）

Background: Cactus contains dietary fiber and minerals and is expected to have preventive effects against diabetes, arteriosclerosis, and other diseases. Additionally, cactus intake induces the production of short-chain fatty acids derived from the gut microbiota, which might influence immune functions. In this study, we examined the effects of a cactus (Nopalea cochenillifera: NC)-supplemented diet on lipopolysaccharide (LPS)-induced immune responses and intestinal barrier function. Methods: Male C3H/HeN mice were randomly divided into three groups—no fiber (NF), cellulose-containing fiber (Cellu), and cactus-added (NC) diets—for 6 weeks. The TNF-α and IL-10 responses to LPS, antibody titers, and intestinal barrier function, as well as the fecal microbiota, were analyzed. Results: The plasma TNF-α but not the IL-10 concentrations were significantly higher in the NC group than in the NF and Cellu groups. Furthermore, the plasma IgG antibody titers were significantly higher in the NC group than in the other groups. The NC group showed higher mucin content and IgA antibody titers in their feces compared with the Cellu group. The succinate and lactate contents, which induce a reduction in TNF-α secretion by macrophages, in the cecum of the NC group were significantly lower than those in the Cellu and NF groups. In contrast, the butyrate content was significantly higher in the cecum of the NC group compared to that of the Cellu group, with a significantly higher relative abundance of butyrate-producing bacteria. Conclusions: Taken together, we found that cactus intake regulates innate and adaptive immune function via the gut microbiota in mice. Therefore, cactus supplementation might serve as a strategy to develop novel functional foods with dietary fiber.

DOI： 10.3390/nu16244376

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担当区分：最終著者,　責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）

記述言語：英語   掲載種別：研究論文（学術雑誌）

記述言語：英語   掲載種別：研究論文（学術雑誌）

Although regular exercise has been reported to prevent depression, it has not been clarified whether the gut microbiota is involved in the factors that prevent depression through exercise. We investigated the effects of voluntary exercise on the gut microbiota and the prevention of depression-like behaviors using mice. C57BL/6 J male mice were subjected to 10 weeks of sedentary control or wheel running, then they were subjected to social defeat stress ( SDS ) . Exercise attenuated that sucrose drinking was decreased by SDS treatment. Exercise increased the expression of Bdnf and decreased expression of Zo-1 and Claudin5 in the brain. Fecal Turicibacter , Allobaculum , and Clostridium sensu stricto , and propionate in the cecum were decreased by the exercise. Voluntary exercise-induced antidepressant properties might be partially caused by suppression of serotonin uptake into gut microbiota and increase the permeability of the blood-brain barrier via reduced propionate production. Graphical Abstract: The depressive behavior is improved by exercise along with high expression of Bdnf in the brain, and changes in Turicibacter and propionate.

DOI： 10.1093/bbb/zbad115

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記述言語：英語   掲載種別：研究論文（学術雑誌）

担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）

Growing evidence from animal experiments suggests that icing after skeletal muscle injury is harmful to muscle regeneration. However, these previous experimental models yielded massive necrotic myofibers, whereas muscle injury with necrosis in a small myofiber fraction (<10%) frequently occurs in human sports activities. Although macrophages play a proreparative role during muscle regeneration, they exert a cytotoxic effect on muscle cells through an inducible nitric oxide synthase (iNOS)-mediated mechanism. In this study, we established an animal injury model with necrosis limited to a small myofiber fraction and investigated the effect of icing on muscle regeneration with a focus on macrophage-related events. Icing after muscle injury of this model resulted in an enlarged size of regenerating myofibers compared with those in untreated animals. During the regenerative process, icing attenuated the accumulation of iNOS-expressing macrophages, suppressed iNOS expression in the whole damaged muscle, and limited the expansion of the injured myofiber area. In addition, icing increased the ratio of M2 macrophages within the injured site at an earlier time point than that in untreated animals. Following these phenomena in icing-treated muscle regeneration, an early accumulation of activated satellite cells within the damaged/regenerating area occurred. The expression level of myogenic regulatory factors, such as MyoD and myogenin, was not affected by icing. Taken together, our results suggest that icing after muscle injury with necrosis limited to a small fraction of myofibers facilitates muscle regeneration by attenuating iNOS-expressing macrophage invasion, limiting muscle damage expansion, and accelerating the accumulation of myogenic cells which form regenerating myofibers.

DOI： 10.1152/ajpregu.00258.2022

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記述言語：英語   掲載種別：研究論文（学術雑誌）

Following skeletal muscle injury, both myogenic and immune cells interact closely during the regenerative process. Although icing is still a common acute treatment for sports-related skeletal muscle injuries, icing after muscle injury has been shown to disrupt macrophage accumulation and impair muscle regeneration in animal models. However, it remains unknown whether icing shortly after injury affects macrophage-related phenomena during the early stages of muscle regeneration. Therefore, we focused on the distribution of M1/M2 macrophages and cytokines expressed predominantly by macrophages during the early stages of muscle regeneration after muscle crush injury. Icing resulted in a decrease, not retardation, in the accumulation of M1 macrophages, but not M2 macrophages, in injured muscles. Consistent with the decrease in M1 macrophage accumulation, icing led to a reduction, instead of delay, in the level of tumor necrosis factor-α (TNF-α) expression. Additionally, at subsequent timepoints, icing decreased the number of myogenic precursor cells in the regenerating area and the size of centrally nucleated regenerating myofibers. Together, our findings suggest that icing after acute muscle damage by crushing disturbs muscle regeneration through hindering tM1 macrophage-related phenomena.

DOI： 10.1007/s00418-022-02143-8

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）

An experimental animal model that causes mild structural disorders of skeletal muscles is essential to understand general exercise-induced muscle damage. Thermal stimulations such as icing and heating are commonly used as treatments for muscle injuries in sports. We established a downhill running (DR) protocol that leads to structural muscle disorders without sarcolemmal disruption and directly compared the structural changes produced by icing and heating after DR. Male ddY mice were divided into the DR, DR plus icing (Ice), and DR plus heating (Heat) groups. All mice ran at 20 m/min, −20% grade on a treadmill for a total of 90 min (three rounds of 30 min). In the Ice and Heat groups, an ice pack and a hot pack were, respectively, applied to the exercised triceps brachii muscles for 20 min just after DR. The proportion of myofibers with structural disorders was higher in the Ice group than in the DR and Heat groups at days 1 and 7 after DR. Moreover, the structural disorder of myofibers was slightly improved in the Heat group at day 1 after DR compared with the DR group. These findings suggest that icing treatment might aggravate the structural changes after DR.

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）

After skeletal muscle injury, unloading disturbs the regenerative process of injured myofibers, in a manner highly attributed to impairment of macrophage functions. However, the effect of unloading on the spatiotemporal context of proinflammatory macrophage recruitment and satellite cell accumulation within the damaged area remains unclear. This study focused on macrophages expressing inducible nitric oxide synthase (iNOS) that synthesize nitric oxide, a key regulator of muscle regeneration, and compared the continuous hindlimb unloading (HU) by tail suspension versus weight-bearing (WB) after skeletal muscle crush injury in rats. We found that in the WB group, the recruitment of iNOS⁺ proinflammatory macrophages into the injured site gradually increased until their peak number at 48 h post-injury. In the HU group, the accumulation of iNOS⁺ macrophages until 48 h after injury was significantly less than that in the WB group and continued to increase at 72 h. In accordance with attenuated and/or delayed iNOS⁺ macrophage recruitment, whole iNOS expression at 24 and 48 h after injury was weakened by unloading. Additionally, in the HU group, satellite cell content of dystrophin-positive non-injured areas diminished at 48 h after injury, and the numbers of activated satellite cells within the regenerating area at 72 and 96 h post-injury were significantly smaller than those in the WB group. These findings suggest that muscle regeneration under unloading conditions results in attenuated and/or delayed recruitment of iNOS⁺ macrophages and lower iNOS expression in the early phase after muscle injury, leading to perturbed satellite cell accumulation and muscle regeneration.

DOI： 10.1007/s00418-020-01897-3

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記述言語：英語   掲載種別：研究論文（学術雑誌）

Migration of the macrophages to the injured site soon after the skeletal muscle injury is crucial for subsequent regeneration of the muscle fibers. The Monocyte chemoattractant protein-1 (MCP-1) is important chemokine for regulating migration of the monocytes/macrophages. Earlier reports have discussed that icing applied soon after muscle crush injury retards muscle regeneration through retardation of macrophage migration. The MCP-1+ cells and neutrophils might promote the migration of the macrophages. To test the hypothesis that icing soon after the skeletal muscle injury affects MCP-1+ cells and neutrophils, we examined the effect of icing on MCP-1+ cells and neutrophils after crush injury to skeletal muscle in rats. Owing to the icing application for 20 min soon after the injury, accumulation of the macrophages was inhibited until 12 h after injury. Numbers of the neutrophils at 3 h after the injury and the MCP-1+ cells at 6 h and later after the injury in the icing group were significantly lower than those in the non-icing group, suggesting that these phenomena contribute to the retardation of macrophage migration.

DOI： 10.1016/j.acthis.2020.151511

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