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Background. Hypothyroid is one of the most frequently known complication of MDR-TB Treatment. Treatment of MDR-TB using Ethionamide still becomes a challenge due to high numbers of patients develop hypothyroid as complication. Studies had reported that Ethionamide (C8H10N2S) share similar sturcture with Thioamides such as Propythiouracil (C7H8N2S) and Methimazole (C4H6N2S), it induced the effect of iodide trapping & organification inhibition which leads to hypothyroidism. However, the molecular mechanism of Ethionamide effects on regulation thyroid hormone receptor gene expression (TR) remains unclear. The understanding of this molecular mechanism, open a new perspective and help to understand the best method of tuberculosis treatment in the future. Purpose. The purpose of this study is to understand molecular mechanism of ethionamide on regulating TRα1, TRα2, TRβ1, and TRβ2 gene expression in gastrocnemius, soleus, thigh, and cardiac muscle. Methods. 38 rats were assigned into 3 groups; negative control group (no treatment), positive control group (propylthiouracyl), treatment group (ethionamide). Each group were given its treatment for 12 weeks. On the last day, all group were sacrificed and organs were sampled (gastrocnemius, soleus, thigh, and cardiac muscle). Each sample were undergone RNA extraction, PCR amplification, and electrophoresis consecutively to analyze the TRα1, TRα2, TRβ1, and TRβ2 gene expression. Result. We observed that TRα1, TRα2, TRβ1, and TRβ2 gene expression were upregulated by 1.5 fold in gastrocnemius muscle, and were upregulated significantly by 3 fold in cardiac muscle. Conclusion. This study concludes that prolong ethionamide treatment does upregulate thyroid hormone receptor gene expression.