MicroRNA-195 (miR-195) was decreased in the patients with pre-eclampsia (PE), which was implicated to modulate PE. Moreover, tissue factor pathway inhibitor 2 (TFPI2), which was highly expressed in the placenta of PE patients, was negatively correlated with miR-195 levels. This study aimed to explore the role of miR-195 in the cell therapy for the treatment of PE and the underlying mechanisms. Human umbilical cord mesenchymal stem cells (hUC-MSCs) were transfected with miR-195 mimic or mimic negative control to extract exosomes. HTR8/SVneo was incubated under hypoxia condition to induce cell damage, and co-co-cultured with exosomes derived from hUC-MSCs to evaluate its effect. Hypoxia time-dependently caused a decrease on miR-195 level with an increase on TFPI2 expression in HTR8/SVneo. MiR-195 directly bind to TFPI2 and inhibited TFPI2 expression in hUC-MSCs. Moreover, hypoxia-induced cell damage in HTR8/SVneo was significantly attenuated by co-culture with hUC-MSC-derived exosomes. Exosomes extracted from miR-195-overexpressed hUC-MSCs, could further ameliorate hypoxia-induced cell damage, due to the excessive amount of miR-195 delivered by exosomes. Exosomal miR-195 in hUC-MSCs alleviated hypoxia-induced cell damage through TFPI2, which might provide a potential therapeutic approach for pre-eclampsia.