An investigation of browsing enrichment, especially non-leaf foraging, on giraffes (Giraffa camelopardalis reticulata) at Kyoto City Zoo in Japan.

Browsing enrichment may aid in developing species-specific behaviors for giraffes managed in zoos as a means of improving animal welfare. By nature, giraffes are tree-feeding animals, including tree bark, but the extent of food other than leaves as a form of browsing enrichment has not been well investigated. Therefore, to investigate the effectiveness of non-leaf foraging, three giraffes at the Kyoto City Zoo in Japan were observed for 228 h from May 2019 to February 2020. In conjunction with behavioral instantaneous sampling, tree use (landscape tree or enrichment branch) and plant part (leaves, twigs, or barks) were recorded by the 1-0 sampling method. There was no significant change in the foraging behavior on the leaves of enriched branches, nor was there any significant change in the foraging behavior of the giraffes, except for one animal in the deciduous phase. No significant changes were observed in rumination or other behaviors between the two phases. Although vegetation foraging behavior significantly decreased, except for one animal, dry hay foraging behavior significantly increased in all the animals during the deciduous phase. Some individuals also showed a significant increase in the foraging behavior for non-leafy parts of the enrichment branches (twigs and bark) during the deciduous phase. This suggests that in some tree species, giraffes forage on the bark and twigs to compensate for the loss of leaves during the deciduous phase, similar to feeding on hay or hay cubes as a substitute for tree leaves.

Effects of browsing enrichment associated with the temperature-humidity index and landscaping trees in giraffes (Giraffa camelopardalisreticulata).

Enclosure environments for captive giraffes can be improved by promoting species-specific behaviors and extending foraging behavior. To date, however, the effects of climatic (temperature-humidity index, THI) and environmental factors (landscaping trees) on the enrichment of captive settings have not been studied. Therefore, the present study explored the effects of browsing enrichment on the licking behavior of captive giraffes. From May 2019 to February 2020, three giraffes in the Kyoto City Zoo, Japan, were observed for 270 h over two consecutive seasons (pre- and post-deciduous). Overall, branch foraging behavior and licking behavior were weakly and negatively correlated. In the pre-deciduous period, THI was significantly and negatively correlated with giraffe activity, and some individuals exhibited significantly reduced foraging behavior. Therefore, browsing enrichment under extreme heat may not improve giraffe rearing environments. Moreover, in the post-deciduous period, with decreased availability of leaves on landscaping trees, the non-branch foraging behavior of giraffes was significantly increased, with a corresponding significant increase in licking behavior. Therefore, landscaping trees affect the foraging behavior of captive giraffes.

Endogenous interleukin-22 prevents cardiac rupture after myocardial infarction in mice.

Myocardial infarction (MI) can result in fatal myocardial rupture or heart failure due to adverse remodeling and dysfunction of the left ventricle. Although recent studies have shown that exogenous interleukin (IL)-22 shows cardioprotective effect after MI, the pathophysiological significance of endogenous IL-22 is unknown. In this study, we investigated the role of endogenous IL-22 in a mouse model of MI. We produced MI model by permanent ligation of the left coronary artery in wild-type (WT) and IL-22 knock-out (KO) mice. The post-MI survival rate was significantly worse in IL-22KO mice than in WT mice due to a higher rate of cardiac rupture. Although IL-22KO mice exhibited a significantly greater infarct size than WT mice, there was no significant difference in left ventricular geometry or function between WT and IL-22KO mice. IL-22KO mice showed increase in infiltrating macrophages and myofibroblasts, and altered expression pattern of inflammation- and extracellular matrix (ECM)-related genes after MI. While IL-22KO mice showed no obvious changes in cardiac morphology or function before MI, expressions of matrix metalloproteinase (MMP)-2 and MMP-9 were increased, whereas that of tissue inhibitor of MMPs (TIMP)-3 was decreased in cardiac tissue. Protein expression of IL-22 receptor complex, IL-22 receptor alpha 1 (IL-22R1) and IL-10 receptor beta (IL-10RB), were increased in cardiac tissue 3 days after MI, regardless of the genotype. We propose that endogenous IL-22 plays an important role in preventing cardiac rupture after MI, possibly by regulating inflammation and ECM metabolism.

SOCS3 deficiency in cardiomyocytes elevates sensitivity of ischemic preconditioning that synergistically ameliorates myocardial ischemia reperfusion injury.

Ischemic preconditioning (IPC) is the most powerful endogenous cardioprotective form of cellular adaptation. However, the inhibitory or augmenting mechanism underlying cardioprotection via IPC remains largely unknown. Suppressor of cytokine signaling-3 (SOCS3) is a cytokine-inducible potent negative feedback regulator of the signal transducer and activator of transcription-3 (STAT3) signaling pathway. Here, we aimed to determine whether cardiac SOCS3 deficiency and IPC would synergistically reduce infarct size after myocardial ischemia reperfusion injury. We evaluated STAT3 activation and SOCS3 induction after ischemic conditioning (IC) using western blot analysis and real-time PCR, and found that myocardial IC alone transiently activated myocardial STAT3 and correspondingly induced SOCS3 expression in wild-type mice. Compared with wild-type mice, cardiac-specific SOCS3 knockout (SOCS3-CKO) mice showed significantly greater and more sustained IC-induced STAT3 activation. Following ischemia reperfusion, IPC substantially reduced myocardial infarct size and significantly enhanced STAT3 phosphorylation in SOCS3-CKO mice compared to in wild-type mice. Real-time PCR array analysis revealed that SOCS3-CKO mice after IC exhibited significantly increased expressions of several anti-apoptotic genes and SAFE pathway-related genes. Moreover, real-time PCR analysis revealed that myocardial IC alone rapidly induced expression of the STAT3-activating cytokine erythropoietin in the kidney at 1 h post-IC. We also found that the circulating erythropoietin level was promptly increased at 1 h after myocardial IC. Myocardial SOCS3 deficiency and IPC exert synergistic effects in the prevention of myocardial injury after ischemia reperfusion. Our present results suggest that myocardial SOCS3 is a potent inhibitor of IPC-induced cardioprotection, and that myocardial SOCS3 inhibition augment IPC-mediated cardioprotection during ischemia reperfusion injury.

Interleukin-22 Directly Activates Myocardial STAT3 (Signal Transducer and Activator of Transcription-3) Signaling Pathway and Prevents Myocardial Ischemia Reperfusion Injury.

BACKGROUND Interleukin (IL)-22, a member of the IL-10 cytokine family, is the only known cytokine that is secreted by immune cells but does not target immune cells; it mainly targets epithelial cells. In this study, we aimed to determine whether IL-22 administration could activate the myocardial STAT3 (signal transducer and activator of transcription-3) signaling pathway, and thus prevent myocardial injury, in a mouse model of ischemia reperfusion injury. METHODS AND RESULTS We evaluated the STAT3 activation after IL-22 injection by Western blot analysis and immunostaining for phosphorylated STAT3 in the heart and found that STAT3 activation in heart tissue rapidly peaked after IL-22 injection. Coimmunostaining of phosphorylated STAT3 and α-actinin revealed that STAT3 activation occurred in cardiomyocytes after IL-22 administration. In heart tissue from intact mice, real-time PCR demonstrated significant expression of IL-22 receptor subunit 1, and coimmunostaining of IL-22 receptor subunit 1 and α-actinin showed IL-22 receptor subunit 1 expression in cardiomyocytes. In cultured cardiomyocytes, IL-22 activated STAT3, and we detected IL-22 receptor subunit 1 expression. Overall, these results indicated that IL-22 directly activated the myocardial IL-22-receptor subunit 1-STAT3 signaling pathway. Following ischemia reperfusion, compared with PBS-treated mice, IL-22-treated mice exhibited a significantly reduced infarct size, significantly reduced myocardial apoptosis, and significantly enhanced phosphorylated STAT3 expression. Moreover, heart tissue from IL-22-treated mice exhibited a significantly reduced expression ratio of phosphorylated p53 to p53. CONCLUSIONS Our present findings suggest that IL-22 directly activated the myocardial STAT3 signaling pathway and acted as a cardioprotective cytokine to ameliorate acute myocardial infarction after ischemia reperfusion.