الفهرس 
Title : Role of angiotensin receptor blockade and chloroquine in experimentally induced osteoporosis
ContentsOnly 14 pages are availabe for public view
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Abstract
Facts that were signified in current study verified the anti-inflammatory capacity of TLM as well as its anti-osteoporotic effect. Turning-off the action of AngII via blocking AT1R contributed to the controlof osteoclastogenesis by eradicating the triggering of ERK protein which subsequently normalized the RANKL/OPG ratio and hence prevented bone degradation. It also replenished BALP, OCN, and calcium levels which subsidize in regulating RANKL activation. These results assured that RAS is involved in the pathogenesis of osteoporosis and confirmed that hindering AT1 receptor by TLM is very likely to have a therapeutic significance.
Chloroquine also showed valuable anti-osteoporotic effects which can be attributed to its inhibitory action on the autophagy-lysosomal pathway thus inhibiting osteoclast differentiation. Furthermore; CQ inhibited ERK protein kinases activation with subsequent decrease in RANKL expression on osteoblastic cells. This decline in RANKL results in an increase in OPG which decreases TRAP and CTSK in the ruffled border of the OCs thus preventing bone degradation