Objective To evaluate the effect of pantoprazole and norepinephrine injection on serum levels of inflammatory factors and hemostasis in the treatment of patients with peptic ulcer bleeding .Methods 102 cases of patients with peptic ulcer bleeding from September 2014 to September 2016 in our hospital were selected and randomly divided into observation group ( n =51 ) and control group ( n =51 ) .Observation group were received pantoprazole and norepinephrine injection combination therapy, the control group received only pantoprazole therapy.The treatment lasted 3 days.The efficacy, bleeding time, hospitalization and blood transfusion, serum IL-6 and IL-10 levels, the incidence of rebleeding and incidence of adverse reactions were compared between two groups.Results The overall response rate ( 98.02%) was significantly higher ( 82.35%) ( P<0.05 );observation group bleeding time was significantly faster than the control group ( P<0.05 ) , length of hospital stay was significantly shorter than the control group (P<0.05), blood transfusion was significantly less than the control group (P<0.05); levels of serum IL-6, IL-10 after treatment were lower than those before treatment (P<0.05); the serum levels of IL-6, IL-10 after treatment were significantly lower than those in control group (P<0.05); rebleeding rate in observation group was significantly lower than that in control group (P<0.05);there was no significant difference in adverse reactions between two groups.Conclusion Pantoprazole and norepinephrine injection in the treatment of digestive bleeding ulcer bleeding has the obvious effect, can reduce serum levels of inflammatory factors, while also reduce the incidence of rebleeding, safe and reliable.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.
Anilides/pharmacology* ; Cerebral Hemorrhage/drug therapy* ; Hematoma/drug therapy* ; Humans ; Macrophages ; Microglia ; Neuroprotection ; PPAR gamma ; Retinoid X Receptor alpha