Anti-HMOX1 polyclonal antibody

Scope Excessive consumption of processed meat has been linked to an increasing risk of gut diseases. It is investigated how pork meat proteins affect colon homeostasis between normal and immune-compromised mice. Methods and results Immune-deficient mice (Rag1(-/-)) and wild-type mice are fed a diet that contains 20% casein or protein isolated from cooked pork or dry-cured pork for 3 months. Rag1(-/-) mice show greater variations in transcriptome responses and higher microbial diversity than wild-type mice after consumption of the pork meat protein diets. Intake of pork meat protein diets also increases body weight and induces colonic oxidative stress, low-grade inflammation, and gene expression involved in immune function, cell cycle, and migration. Key genes like Hmox1, Ppara, and Pparg are highly upregulated by pork meat protein. These changes are associated with decreased abundances of Blautia, Bifidobacterium, and Alistipes and increased abundances of Akkermansia muciniphila and Ruminococcaceae. Conclusion Pork meat proteins affect colon health in both wild-type and Rag1(-/-) mice by altering the microbiome profile under the complex interaction with adaptive immunity. The findings herein give a new insight into the understanding of meat intake, immunity, and gut health.

Background and Purpose-Subarachnoid hemorrhage (SAH) is associated with a temporal pattern of stroke incidence. We hypothesized that natural oscillations in gene expression controlling circadian rhythm affect the severity of neuronal injury. We moreover predict that heme oxygenase-1 (HO-1/Hmox1) and its product carbon monoxide (CO) contribute to the restoration of rhythm and neuroprotection. Methods-Murine SAH model was used where blood was injected at various time points of the circadian cycle. Readouts included circadian clock gene expression, locomotor activity, vasospasm, neuroinflammatory markers, and apoptosis. In addition, cerebrospinal fluid and peripheral blood leukocytes from SAH patients and controls were analyzed for clock gene expression. Results-Significant elevations in the clock genes Per-1, Per-2, and NPAS-2 were observed in the hippocampus, cortex, and suprachiasmatic nucleus in mice subjected to SAH at zeitgeber time (ZT) 12 when compared with ZT2. Clock gene expression amplitude correlated with basal expression of HO-1, which was also significantly greater at ZT12. SAH animals showed a significant reduction in cerebral vasospasm, neuronal apoptosis, and microglial activation at ZT12 compared with ZT2. In animals with myeloid-specific HO-1 deletion (Lyz-Cre-Hmox1(fl/fl)), Per-1, Per-2, and NPAS-2 expression was reduced in the suprachiasmatic nucleus, which correlated with increased injury. Treatment with low-dose CO rescued Lyz-Cre-Hmox1(fl/fl) mice, restored Per-1, Per-2, and NPAS-2 expression, and reduced neuronal apoptosis. Conclusions-Clock gene expression regulates, in part, the severity of SAH and requires myeloid HO-1 activity to clear the erythrocyte burden and inhibit neuronal apoptosis. Exposure to CO rescues the loss of HO-1 and thus merits further investigation in patients with SAH.