Abstract:Background/objectives
Adipose tissue macrophages (ATMs) exist in either the M1 or M2 form. The anti-inflammatory M2 ATMs accumulate in lean individuals, whereas the pro-inflammatory M1 ATMs accumulate in obese individuals. Bee venom phospholipase A2 (bvPLA2), a major component in honeybee (Apis mellifera) venom, exerts potent anti-inflammatory effects via interactions with regulatory T cells (Treg) and macrophages. This study investigated the effects of bvPLA2 on a high-fat diet (HFD)-induced obe… Show more
“…It has been shown that bvPLA2 protected against acetaminophen-induced acute liver injury in mice [13]. In addition, a recent study reported that bvPLA2 attenuated obesity-associated hepatotoxicity in high fat diet-induced obese mice [25]. Taken together, these results suggest that bvPLA2 may have therapeutic effects not only in acute liver injury, but also chronic liver disease.…”
Hepatocyte apoptosis and inflammation play important roles in cholestatic liver diseases. Bee venom-derived secretory phospholipase A2 (bvPLA2) has been shown to ameliorate various inflammatory diseases. However, whether bvPLA2 has a therapeutic effect against cholestatic liver disease has not been evaluated. Therefore, we investigated the effects of bvPLA2 on cholestatic liver injury and fibrosis in a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding. The administration of bvPLA2 ameliorated liver damage, cholestasis, and fibrosis in DDC diet-fed mice, as assessed by serum biochemical tests and histological examinations. In addition, bvPLA2 reduced myofibroblast accumulation, concomitant with suppression of transforming growth factor-β signaling cascade. The administration of bvPLA2 inhibited hepatocyte apoptosis in DDC diet-fed mice as represented by a reduction in the number of cells stained with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and suppression of caspase-3 activation. Moreover, bvPLA2 reduced cytokine production along with the inhibition of the nuclear factor kappa-B pathway. The number of regulatory T-cells was increased by bvPLA2, while the number of other immune cells, including neutrophils, macrophages, and CD8+ T-cells, was decreased. Our data indicate that the administration of bvPLA2 ameliorates cholestatic liver injury and fibrosis by inhibiting hepatocyte apoptosis and inflammation.
“…It has been shown that bvPLA2 protected against acetaminophen-induced acute liver injury in mice [13]. In addition, a recent study reported that bvPLA2 attenuated obesity-associated hepatotoxicity in high fat diet-induced obese mice [25]. Taken together, these results suggest that bvPLA2 may have therapeutic effects not only in acute liver injury, but also chronic liver disease.…”
Hepatocyte apoptosis and inflammation play important roles in cholestatic liver diseases. Bee venom-derived secretory phospholipase A2 (bvPLA2) has been shown to ameliorate various inflammatory diseases. However, whether bvPLA2 has a therapeutic effect against cholestatic liver disease has not been evaluated. Therefore, we investigated the effects of bvPLA2 on cholestatic liver injury and fibrosis in a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding. The administration of bvPLA2 ameliorated liver damage, cholestasis, and fibrosis in DDC diet-fed mice, as assessed by serum biochemical tests and histological examinations. In addition, bvPLA2 reduced myofibroblast accumulation, concomitant with suppression of transforming growth factor-β signaling cascade. The administration of bvPLA2 inhibited hepatocyte apoptosis in DDC diet-fed mice as represented by a reduction in the number of cells stained with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and suppression of caspase-3 activation. Moreover, bvPLA2 reduced cytokine production along with the inhibition of the nuclear factor kappa-B pathway. The number of regulatory T-cells was increased by bvPLA2, while the number of other immune cells, including neutrophils, macrophages, and CD8+ T-cells, was decreased. Our data indicate that the administration of bvPLA2 ameliorates cholestatic liver injury and fibrosis by inhibiting hepatocyte apoptosis and inflammation.
“…Mas aun, se aumenta la concentración circulante de leptina y se reduce la adiponectina, condición que se torna crónica, y se desenlaza un cuadro proinflamatorio de bajo grado que, a mediano o largo plazo, desencadena respuestas de resistencia a la insulina, hipertensión, diabetes tipo 2, síndrome metabólico, enfermedades cardiovasculares e, incluso, cáncer 25. La quemerina es una adipocina inflamatoria asociada con aumento en la ingesta de alimentos que también ha sido implicada en la promoción de angiogénesis, hiperplasia, hipertrofia en tejido adiposo blanco, pero no en el marrón (Jeong et al, 2021). Interesantemente, se ha encontrado que las células grasas de animales obesos producen grandes cantidades de MCP-1, sustancia que atrae macrófagos al tejido graso 26.…”
Existen diversos estímulos que pueden conllevar al desarrollo de inflamación. La inflamación generalmente se define como una respuesta localizada subsecuente a un daño ocasionado en el tejido, puede subdividirse en aguda o crónica, según la duración. El agente nocivo puede ser externo, de naturaleza química, física, o biológica. La respuesta inflamatoria involucra diferentes células del sistema inmune y la producción de una amplia variedad de moléculas. Algunos fármacos como el celecoxib y rofecoxib tienen su aplicación en inflamación crónica, disminuyendo la respuesta inflamatoria, pero generando efectos adversos leves o moderados debido a la inespecificidad de los fármacos o por reacciones adversas de éstos. La obesidad consiste en el incremento del peso corporal asociado a un desequilibrio calórico. El aumento en peso corporal está relacionado a un incremento en la masa de tejido adiposo graso distribuido en diferentes depósitos del organismo. El desarrollo de obesidad se considera multifactorial y conlleva el riesgo de generar consecuencias graves tanto en la salud como en la calidad de vida de las personas. Ya que la obesidad conlleva a un estado de inflamación crónico de bajo grado, esta también se asocia con el desarrollo de condiciones crónicas, entre las cuales destacan el síndrome metabólico, enfermedades cardiovasculares, diabetes, problemas respiratorios, cáncer, y recientemente ha sobresalido como un factor de riesgo del desarrollo de un cuadro COVID-19 agresivo. En nuestro país, se calcula que más de la mitad de la población adulta sufre de sobrepeso, cifra que tiene una tendencia al aumento y que posiciona a la obesidad como la epidemia de la próxima década.
“…As a result, low-grade inflammation in overweight people is influenced in part by dietary factors. In a high-fat diet (HFD) induced obesity model, increased infiltration of immune cell - inflammatory macrophages (type M1) - in adipose tissues, which is linked to an increase in inflammatory cytokines [35] . After the three weeks of HFD treatment onwards, an increase in macrophage-related genes was detected, and after the sixteen weeks ahead, the increase became more pronounced, culminating in the commencement of insulin resistance 35 , 36 .…”
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