Activation of M3 Muscarinic Acetylcholine Receptors Delayed Cardiac Aging by Inhibiting the Caspase-1/IL-1β Signaling Pathway.

Background/aims: Because the prevalence of age-related cardiac impairment increases as the human lifespan increases, it is important to combat the effects of aging. Recently, the cardiac M3 muscarinic acetylcholine receptor (M3-mAChR) has been demonstrated to play important roles in cardiac development and in the pathogenesis of cardiac diseases. However, the role of M3-mAChR in aging remains largely unknown.

[Effects of HS 6101 and rhG-CSF on Hematopoiesis Recovery of ICR Mice Injured by Cyclophosphamide].

Objective: To investigate the effects of HS 6101 and recombinant human granulocyte colony stimulating factor (rhG-CSF) on hematopoiesis recovery of ICR mice injured by cyclophosphamide (CTX).

Methods: A total of 103 ICR mice were divided into 4 groups, including CTX control (46 mice), HS 6101 (21 mice), rhG-CSF (18 mice) and HS 6101+rhG-CSF (18 mice), respectively. The mouse model of chemotherapy-induced haematopoietic injury was established by CTX intraperitoneal injection at a dose of 100 mg/kg once a day for 3 consecutive days.

[Protective effect of HS-6101 on rhesus monkeys with severe hematopoietic acute radiation sickness].

This study was purposed to investigate the protective effects of lipoprotein HS-6101(6101) on rhesus monkey total body irradiated with 7.0 Gy ⁶⁰Coγ-ray. A total of 30 health adult rhesus monkeys were randomly divided into symptomatic therapy (ST), WR2721 and HS-6101 30, 90 and 270 mg/kg groups (n = 6), the rhesus monkeys of each groups were injected with physiological saline 0.

Characterization of the excitatory mechanism induced by Jingzhaotoxin-I inhibiting sodium channel inactivation.

We have recently isolated a peptide neurotoxin, Jingzhaotoxin-I (JZTX-I), from Chinese tarantula Chilobrachys jingzhao venom that preferentially inhibits cardiac sodium channel inactivation and may define a new subclass of spider sodium channel toxins. In this study, we found that in contrast to other spider sodium channel toxins acting presynaptically rather than postsynaptically, JZTX-I augmented frog end-plate potential amplitudes and caused an increase in both nerve mediated and unmediated muscle twitches. Although JZTX-I does not negatively shift sodium channel activation threshold, an evident increase in muscle fasciculation was detected.